Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice

Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decr...
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Autor*in:	Tsunoda, Michinori [verfasserIn] Matsuo, Ichiro Ohnuki, Yoshiki Suita, Kenji Ishikawa, Misao Mitsubayashi, Takao Ito, Aiko Mototani, Yasumasa Kiyomoto, Kenichi Morii, Akinaka Nariyama, Megumi Hayakawa, Yoshio Gomi, Kazuhiro Okumura, Satoshi

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	β-Adrenergic signaling Periodontitis Adenylyl cyclase Apoptosis Fibrosis Signal transduction Heart failure

Anmerkung:	© The Author(s) 2023

Übergeordnetes Werk:	Enthalten in: The journal of physiological sciences - [Tokyo] : Springer, 2006, 73(2023), 1 vom: 09. Aug.
Übergeordnetes Werk:	volume:73 ; year:2023 ; number:1 ; day:09 ; month:08

Links:	Volltext

DOI / URN:	10.1186/s12576-023-00873-5

Katalog-ID:	SPR052686213

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allfields	10.1186/s12576-023-00873-5 doi (DE-627)SPR052686213 (SPR)s12576-023-00873-5-e DE-627 ger DE-627 rakwb eng Tsunoda, Michinori verfasserin aut Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease. β-Adrenergic signaling (dpeaa)DE-He213 Periodontitis (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Matsuo, Ichiro aut Ohnuki, Yoshiki aut Suita, Kenji aut Ishikawa, Misao aut Mitsubayashi, Takao aut Ito, Aiko aut Mototani, Yasumasa aut Kiyomoto, Kenichi aut Morii, Akinaka aut Nariyama, Megumi aut Hayakawa, Yoshio aut Gomi, Kazuhiro aut Okumura, Satoshi (orcid)0000-0001-8747-7941 aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 73(2023), 1 vom: 09. Aug. (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:73 year:2023 number:1 day:09 month:08 https://dx.doi.org/10.1186/s12576-023-00873-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2014 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 73 2023 1 09 08
spelling	10.1186/s12576-023-00873-5 doi (DE-627)SPR052686213 (SPR)s12576-023-00873-5-e DE-627 ger DE-627 rakwb eng Tsunoda, Michinori verfasserin aut Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease. β-Adrenergic signaling (dpeaa)DE-He213 Periodontitis (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Matsuo, Ichiro aut Ohnuki, Yoshiki aut Suita, Kenji aut Ishikawa, Misao aut Mitsubayashi, Takao aut Ito, Aiko aut Mototani, Yasumasa aut Kiyomoto, Kenichi aut Morii, Akinaka aut Nariyama, Megumi aut Hayakawa, Yoshio aut Gomi, Kazuhiro aut Okumura, Satoshi (orcid)0000-0001-8747-7941 aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 73(2023), 1 vom: 09. Aug. (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:73 year:2023 number:1 day:09 month:08 https://dx.doi.org/10.1186/s12576-023-00873-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2014 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 73 2023 1 09 08
allfields_unstemmed	10.1186/s12576-023-00873-5 doi (DE-627)SPR052686213 (SPR)s12576-023-00873-5-e DE-627 ger DE-627 rakwb eng Tsunoda, Michinori verfasserin aut Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease. β-Adrenergic signaling (dpeaa)DE-He213 Periodontitis (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Matsuo, Ichiro aut Ohnuki, Yoshiki aut Suita, Kenji aut Ishikawa, Misao aut Mitsubayashi, Takao aut Ito, Aiko aut Mototani, Yasumasa aut Kiyomoto, Kenichi aut Morii, Akinaka aut Nariyama, Megumi aut Hayakawa, Yoshio aut Gomi, Kazuhiro aut Okumura, Satoshi (orcid)0000-0001-8747-7941 aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 73(2023), 1 vom: 09. Aug. (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:73 year:2023 number:1 day:09 month:08 https://dx.doi.org/10.1186/s12576-023-00873-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2014 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 73 2023 1 09 08
allfieldsGer	10.1186/s12576-023-00873-5 doi (DE-627)SPR052686213 (SPR)s12576-023-00873-5-e DE-627 ger DE-627 rakwb eng Tsunoda, Michinori verfasserin aut Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease. β-Adrenergic signaling (dpeaa)DE-He213 Periodontitis (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Matsuo, Ichiro aut Ohnuki, Yoshiki aut Suita, Kenji aut Ishikawa, Misao aut Mitsubayashi, Takao aut Ito, Aiko aut Mototani, Yasumasa aut Kiyomoto, Kenichi aut Morii, Akinaka aut Nariyama, Megumi aut Hayakawa, Yoshio aut Gomi, Kazuhiro aut Okumura, Satoshi (orcid)0000-0001-8747-7941 aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 73(2023), 1 vom: 09. Aug. (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:73 year:2023 number:1 day:09 month:08 https://dx.doi.org/10.1186/s12576-023-00873-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2014 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 73 2023 1 09 08
allfieldsSound	10.1186/s12576-023-00873-5 doi (DE-627)SPR052686213 (SPR)s12576-023-00873-5-e DE-627 ger DE-627 rakwb eng Tsunoda, Michinori verfasserin aut Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023 Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease. β-Adrenergic signaling (dpeaa)DE-He213 Periodontitis (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213 Matsuo, Ichiro aut Ohnuki, Yoshiki aut Suita, Kenji aut Ishikawa, Misao aut Mitsubayashi, Takao aut Ito, Aiko aut Mototani, Yasumasa aut Kiyomoto, Kenichi aut Morii, Akinaka aut Nariyama, Megumi aut Hayakawa, Yoshio aut Gomi, Kazuhiro aut Okumura, Satoshi (orcid)0000-0001-8747-7941 aut Enthalten in The journal of physiological sciences [Tokyo] : Springer, 2006 73(2023), 1 vom: 09. Aug. (DE-627)572081235 (DE-600)2437104-X 1880-6562 nnns volume:73 year:2023 number:1 day:09 month:08 https://dx.doi.org/10.1186/s12576-023-00873-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2014 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 73 2023 1 09 08
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author	Tsunoda, Michinori
spellingShingle	Tsunoda, Michinori misc β-Adrenergic signaling misc Periodontitis misc Adenylyl cyclase misc Apoptosis misc Fibrosis misc Signal transduction misc Heart failure Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice
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topic_title	Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice β-Adrenergic signaling (dpeaa)DE-He213 Periodontitis (dpeaa)DE-He213 Adenylyl cyclase (dpeaa)DE-He213 Apoptosis (dpeaa)DE-He213 Fibrosis (dpeaa)DE-He213 Signal transduction (dpeaa)DE-He213 Heart failure (dpeaa)DE-He213
topic	misc β-Adrenergic signaling misc Periodontitis misc Adenylyl cyclase misc Apoptosis misc Fibrosis misc Signal transduction misc Heart failure
topic_unstemmed	misc β-Adrenergic signaling misc Periodontitis misc Adenylyl cyclase misc Apoptosis misc Fibrosis misc Signal transduction misc Heart failure
topic_browse	misc β-Adrenergic signaling misc Periodontitis misc Adenylyl cyclase misc Apoptosis misc Fibrosis misc Signal transduction misc Heart failure
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title	Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice
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title_full	Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice
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author_browse	Tsunoda, Michinori Matsuo, Ichiro Ohnuki, Yoshiki Suita, Kenji Ishikawa, Misao Mitsubayashi, Takao Ito, Aiko Mototani, Yasumasa Kiyomoto, Kenichi Morii, Akinaka Nariyama, Megumi Hayakawa, Yoshio Gomi, Kazuhiro Okumura, Satoshi
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title_sort	vidarabine, an anti-herpes agent, improves porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice
title_auth	Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice
abstract	Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease. © The Author(s) 2023
abstractGer	Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease. © The Author(s) 2023
abstract_unstemmed	Abstract In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease. © The Author(s) 2023
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title_short	Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice
url	https://dx.doi.org/10.1186/s12576-023-00873-5
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author2	Matsuo, Ichiro Ohnuki, Yoshiki Suita, Kenji Ishikawa, Misao Mitsubayashi, Takao Ito, Aiko Mototani, Yasumasa Kiyomoto, Kenichi Morii, Akinaka Nariyama, Megumi Hayakawa, Yoshio Gomi, Kazuhiro Okumura, Satoshi
author2Str	Matsuo, Ichiro Ohnuki, Yoshiki Suita, Kenji Ishikawa, Misao Mitsubayashi, Takao Ito, Aiko Mototani, Yasumasa Kiyomoto, Kenichi Morii, Akinaka Nariyama, Megumi Hayakawa, Yoshio Gomi, Kazuhiro Okumura, Satoshi
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up_date	2024-07-03T14:03:44.419Z
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Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/$ Ca^{2+} $-calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. 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Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice

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