Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy
Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac h...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhong, Beihua [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018transfer abstract |
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| Schlagwörter: |
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| Umfang: |
10 |
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| Übergeordnetes Werk: |
Enthalten in: A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a - Liao, Gary ELSEVIER, 2020, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:99 ; year:2018 ; pages:261-270 ; extent:10 |
| Links: |
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| DOI / URN: |
10.1016/j.biopha.2018.01.065 |
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ELV04201400X |
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| 245 | 1 | 0 | |a Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy |
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| 520 | |a Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. | ||
| 520 | |a Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. | ||
| 650 | 7 | |a Heart |2 Elsevier | |
| 650 | 7 | |a Inflammation |2 Elsevier | |
| 650 | 7 | |a TRPV1 |2 Elsevier | |
| 650 | 7 | |a Hypertrophy |2 Elsevier | |
| 650 | 7 | |a Macrophage |2 Elsevier | |
| 700 | 1 | |a Rubinstein, Jack |4 oth | |
| 700 | 1 | |a Ma, Shuangtao |4 oth | |
| 700 | 1 | |a Wang, Donna H. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Liao, Gary ELSEVIER |t A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a |d 2020 |g Amsterdam [u.a.] |w (DE-627)ELV004620771 |
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10.1016/j.biopha.2018.01.065 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001691.pica (DE-627)ELV04201400X (ELSEVIER)S0753-3322(17)35062-X DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Zhong, Beihua verfasserin aut Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy 2018transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Heart Elsevier Inflammation Elsevier TRPV1 Elsevier Hypertrophy Elsevier Macrophage Elsevier Rubinstein, Jack oth Ma, Shuangtao oth Wang, Donna H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:99 year:2018 pages:261-270 extent:10 https://doi.org/10.1016/j.biopha.2018.01.065 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 99 2018 261-270 10 |
| spelling |
10.1016/j.biopha.2018.01.065 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001691.pica (DE-627)ELV04201400X (ELSEVIER)S0753-3322(17)35062-X DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Zhong, Beihua verfasserin aut Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy 2018transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Heart Elsevier Inflammation Elsevier TRPV1 Elsevier Hypertrophy Elsevier Macrophage Elsevier Rubinstein, Jack oth Ma, Shuangtao oth Wang, Donna H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:99 year:2018 pages:261-270 extent:10 https://doi.org/10.1016/j.biopha.2018.01.065 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 99 2018 261-270 10 |
| allfields_unstemmed |
10.1016/j.biopha.2018.01.065 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001691.pica (DE-627)ELV04201400X (ELSEVIER)S0753-3322(17)35062-X DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Zhong, Beihua verfasserin aut Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy 2018transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Heart Elsevier Inflammation Elsevier TRPV1 Elsevier Hypertrophy Elsevier Macrophage Elsevier Rubinstein, Jack oth Ma, Shuangtao oth Wang, Donna H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:99 year:2018 pages:261-270 extent:10 https://doi.org/10.1016/j.biopha.2018.01.065 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 99 2018 261-270 10 |
| allfieldsGer |
10.1016/j.biopha.2018.01.065 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001691.pica (DE-627)ELV04201400X (ELSEVIER)S0753-3322(17)35062-X DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Zhong, Beihua verfasserin aut Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy 2018transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Heart Elsevier Inflammation Elsevier TRPV1 Elsevier Hypertrophy Elsevier Macrophage Elsevier Rubinstein, Jack oth Ma, Shuangtao oth Wang, Donna H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:99 year:2018 pages:261-270 extent:10 https://doi.org/10.1016/j.biopha.2018.01.065 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 99 2018 261-270 10 |
| allfieldsSound |
10.1016/j.biopha.2018.01.065 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001691.pica (DE-627)ELV04201400X (ELSEVIER)S0753-3322(17)35062-X DE-627 ger DE-627 rakwb eng 610 VZ 44.86 bkl Zhong, Beihua verfasserin aut Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy 2018transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. Heart Elsevier Inflammation Elsevier TRPV1 Elsevier Hypertrophy Elsevier Macrophage Elsevier Rubinstein, Jack oth Ma, Shuangtao oth Wang, Donna H. oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:99 year:2018 pages:261-270 extent:10 https://doi.org/10.1016/j.biopha.2018.01.065 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 99 2018 261-270 10 |
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genetic ablation of trpv1 exacerbates pressure overload-induced cardiac hypertrophy |
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Genetic ablation of TRPV1 exacerbates pressure overload-induced cardiac hypertrophy |
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Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. |
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Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. |
| abstract_unstemmed |
Transient receptor potential vanilloid 1 (TRPV1) channels expressed in sensory nerves may regulate vascular tone and cardiovascular function via their anti-inflammatory effects by releasing neuropeptide calcitonin gene-related peptide (CGRP). Inflammation plays a role in the progression of cardiac hypertrophy and TRPV1 activation may be key to cardiac inflammatory processes. The aim of this study was to test the hypothesis that TRPV1 modulates inflammatory processes to protect the heart from pressure overload-induced hypertrophy and inflammatory responses. Trpv1 knockout (Trpv1 −/−) and wild-type (WT) mice were subjected to transverse aortic constriction (TAC) or sham operation. Four weeks after TAC, WT and Trpv1 -/- mice had developed left ventricular (LV) hypertrophy with increased LV mass, fibrosis and infiltration of macrophages as well as increased secretion of tumor necrosis factor α, interleukin-6 from cardiac tissue (all P < 0.05), those were higher in Trpv1 -/- than in WT mice with TAC (all P < 0.05). In addition, decreases of LV ejection fraction and fractional shortening were greater in Trpv1 -/- than in WT mice (both P < 0.05). Moreover, atrial natriuretic peptide level was greater in Trpv1 -/- than in WT mice with TAC (P < 0.05). Compared to sham control, TAC procedure significantly increased cardiac TRPV1 expression and CGRP release in WT mice (both P < 0.05), but not in Trpv1 -/- mice. These results demonstrate that Trpv1 gene deletion results in excessive inflammation, exaggerates cardiac hypertrophy, and deteriorates cardiac function after TAC, which may be due to abnormal cardiac remodeling and decreased CGRP in the absence of TRPV1. |
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