Association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: A systematic review and meta-analysis of in vitro, in vivo and human studies
To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sophocleous, Antonia [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China - Deng, Lixing ELSEVIER, 2022, the official journal of the Italian Pharmacological Society, London |
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| Übergeordnetes Werk: |
volume:175 ; year:2022 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.phrs.2021.105928 |
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ELV056452209 |
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| 245 | 1 | 0 | |a Association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: A systematic review and meta-analysis of in vitro, in vivo and human studies |
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| 520 | |a To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. | ||
| 520 | |a To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. | ||
| 650 | 7 | |a CB2 |2 Elsevier | |
| 650 | 7 | |a Cannabis |2 Elsevier | |
| 650 | 7 | |a CB1 |2 Elsevier | |
| 650 | 7 | |a Osteoblast |2 Elsevier | |
| 650 | 7 | |a Osteoclast |2 Elsevier | |
| 650 | 7 | |a Bone |2 Elsevier | |
| 700 | 1 | |a Yiallourides, Michael |4 oth | |
| 700 | 1 | |a Zeng, Feier |4 oth | |
| 700 | 1 | |a Pantelas, Pantelis |4 oth | |
| 700 | 1 | |a Stylianou, Eleni |4 oth | |
| 700 | 1 | |a Li, Boya |4 oth | |
| 700 | 1 | |a Carrasco, Giovana |4 oth | |
| 700 | 1 | |a Idris, Aymen I. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Academic Press |a Deng, Lixing ELSEVIER |t Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China |d 2022 |d the official journal of the Italian Pharmacological Society |g London |w (DE-627)ELV008224951 |
| 773 | 1 | 8 | |g volume:175 |g year:2022 |g pages:0 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.phrs.2021.105928 |3 Volltext |
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10.1016/j.phrs.2021.105928 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001638.pica (DE-627)ELV056452209 (ELSEVIER)S1043-6618(21)00512-0 DE-627 ger DE-627 rakwb eng 330 VZ Sophocleous, Antonia verfasserin aut Association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: A systematic review and meta-analysis of in vitro, in vivo and human studies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. CB2 Elsevier Cannabis Elsevier CB1 Elsevier Osteoblast Elsevier Osteoclast Elsevier Bone Elsevier Yiallourides, Michael oth Zeng, Feier oth Pantelas, Pantelis oth Stylianou, Eleni oth Li, Boya oth Carrasco, Giovana oth Idris, Aymen I. oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:175 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2021.105928 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 175 2022 0 |
| spelling |
10.1016/j.phrs.2021.105928 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001638.pica (DE-627)ELV056452209 (ELSEVIER)S1043-6618(21)00512-0 DE-627 ger DE-627 rakwb eng 330 VZ Sophocleous, Antonia verfasserin aut Association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: A systematic review and meta-analysis of in vitro, in vivo and human studies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. CB2 Elsevier Cannabis Elsevier CB1 Elsevier Osteoblast Elsevier Osteoclast Elsevier Bone Elsevier Yiallourides, Michael oth Zeng, Feier oth Pantelas, Pantelis oth Stylianou, Eleni oth Li, Boya oth Carrasco, Giovana oth Idris, Aymen I. oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:175 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2021.105928 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 175 2022 0 |
| allfields_unstemmed |
10.1016/j.phrs.2021.105928 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001638.pica (DE-627)ELV056452209 (ELSEVIER)S1043-6618(21)00512-0 DE-627 ger DE-627 rakwb eng 330 VZ Sophocleous, Antonia verfasserin aut Association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: A systematic review and meta-analysis of in vitro, in vivo and human studies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. CB2 Elsevier Cannabis Elsevier CB1 Elsevier Osteoblast Elsevier Osteoclast Elsevier Bone Elsevier Yiallourides, Michael oth Zeng, Feier oth Pantelas, Pantelis oth Stylianou, Eleni oth Li, Boya oth Carrasco, Giovana oth Idris, Aymen I. oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:175 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2021.105928 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 175 2022 0 |
| allfieldsGer |
10.1016/j.phrs.2021.105928 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001638.pica (DE-627)ELV056452209 (ELSEVIER)S1043-6618(21)00512-0 DE-627 ger DE-627 rakwb eng 330 VZ Sophocleous, Antonia verfasserin aut Association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: A systematic review and meta-analysis of in vitro, in vivo and human studies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. CB2 Elsevier Cannabis Elsevier CB1 Elsevier Osteoblast Elsevier Osteoclast Elsevier Bone Elsevier Yiallourides, Michael oth Zeng, Feier oth Pantelas, Pantelis oth Stylianou, Eleni oth Li, Boya oth Carrasco, Giovana oth Idris, Aymen I. oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:175 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2021.105928 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 175 2022 0 |
| allfieldsSound |
10.1016/j.phrs.2021.105928 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001638.pica (DE-627)ELV056452209 (ELSEVIER)S1043-6618(21)00512-0 DE-627 ger DE-627 rakwb eng 330 VZ Sophocleous, Antonia verfasserin aut Association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: A systematic review and meta-analysis of in vitro, in vivo and human studies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. CB2 Elsevier Cannabis Elsevier CB1 Elsevier Osteoblast Elsevier Osteoclast Elsevier Bone Elsevier Yiallourides, Michael oth Zeng, Feier oth Pantelas, Pantelis oth Stylianou, Eleni oth Li, Boya oth Carrasco, Giovana oth Idris, Aymen I. oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:175 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2021.105928 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 175 2022 0 |
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We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. 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association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: a systematic review and meta-analysis of in vitro, in vivo and human studies |
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Association of cannabinoid receptor modulation with normal and abnormal skeletal remodelling: A systematic review and meta-analysis of in vitro, in vivo and human studies |
| abstract |
To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. |
| abstractGer |
To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. |
| abstract_unstemmed |
To address the inconsistent findings from studies that used different models to explore the role of classical cannabinoid type 1 (CB1) and 2 (CB2) receptors in skeletal remodelling, we searched Medline, Web of Science and Embase for relevant studies from inception to June 23, 2020. We identified 38 in vitro, 34 in vivo and 9 human studies. A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models. |
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A meta-analysis of in vitro studies showed that exposure to the inverse-agonists AM251 (mean difference [MD]:−26.75, 95% confidence interval [CI]:−45.36,−8.14, p = 0.005), AM630 (standardised[std.] MD:−3.11, CI:−5.26,−0.97, p = 0.004; SR144528, std.MD:−4.88, CI −7.58,−2.18, p = 0.0004) and CBD (std.MD:−1.39, CI −2.64,−0.14, p = 0.03) is associated with reduced osteoclastogenesis, whereas the endocannabinoid 2-AG (std.MD:2.00, CI:0.11–3.89, p = 0.04) and CB2-selective agonist HU308 (MD:19.38, CI:11.75–27.01, p < 0.00001) were stimulatory. HU308 also enhanced osteoblast differentiation (std.MD:2.22, CI:0.95–3.50, p = 0.0006) and activity (std.MD:2.97, CI:1.22–4.71, p = 0.0008). In models of bone loss, CB1/2 deficiency enhanced peak bone volume (std.MD:3.70, CI:1.77–5.63, p = 0.0002) but reduced bone formation (std.MD:−0.54, CI:−0.90,−0.17, p = 0.004) in female mice. In male rats, CB1/2 deficiency (std.MD:2.31, CI:0.30–4.33, p = 0.02) and AM251 or CBD treatments (std.MD:2.19, CI:0.46–3.93, p = 0.01) enhanced bone volume. CB1/2 deficiency (std.MD:9.78, CI:4.96–14.61, p < 0.0001) and AM251 or AM630 treatments (std.MD:28.19, CI:19.13–37.25, p < 0.0001) were associated with osteoprotection. The CB2-selective agonists JWH133 and 4Q3C enhanced bone volume in arthritic rodents (std.MD:14.45, CI:2.08–26.81, p = 0.02). In human, CB2 SNPs (AA:rs2501431, MD:−0.28, CI:−0.55,−0.01, p = 0.04; CC:rs2501432, MD:−0.29, CI:−0.56,−0.02, p = 0.03) were associated with reduced bone mineral density, however the association of Marijuana use remains unclear. Thus, CB1/2 modulation is associated with altered bone metabolism, however findings are confounded by low study number and heterogenicity of models.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CB2</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Cannabis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">CB1</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Osteoblast</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Osteoclast</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Bone</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yiallourides, Michael</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zeng, Feier</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Pantelas, Pantelis</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Stylianou, Eleni</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Li, Boya</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Carrasco, Giovana</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Idris, Aymen I.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="a">Deng, Lixing ELSEVIER</subfield><subfield code="t">Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China</subfield><subfield code="d">2022</subfield><subfield code="d">the official journal of the Italian Pharmacological Society</subfield><subfield code="g">London</subfield><subfield code="w">(DE-627)ELV008224951</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:175</subfield><subfield code="g">year:2022</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.phrs.2021.105928</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">175</subfield><subfield code="j">2022</subfield><subfield code="h">0</subfield></datafield></record></collection>
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