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Melatonin ameliorates PM(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis

Fine particulate matter (PM(2.5)) exposure is correlated with the risk of developing cardiac fibrosis. Melatonin is a major secretory product of the pineal gland that has been reported to prevent fibrosis. However, whether melatonin affects the adverse health effects of PM(2.5) exposure has not been...

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Autores principales: Jiang, Jinjin, Liang, Shuang, Zhang, Jingyi, Du, Zhou, Xu, Qing, Duan, Junchao, Sun, Zhiwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7757260/
https://www.ncbi.nlm.nih.gov/pubmed/32730639
http://dx.doi.org/10.1111/jpi.12686
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author Jiang, Jinjin
Liang, Shuang
Zhang, Jingyi
Du, Zhou
Xu, Qing
Duan, Junchao
Sun, Zhiwei
author_facet Jiang, Jinjin
Liang, Shuang
Zhang, Jingyi
Du, Zhou
Xu, Qing
Duan, Junchao
Sun, Zhiwei
author_sort Jiang, Jinjin
collection PubMed
description Fine particulate matter (PM(2.5)) exposure is correlated with the risk of developing cardiac fibrosis. Melatonin is a major secretory product of the pineal gland that has been reported to prevent fibrosis. However, whether melatonin affects the adverse health effects of PM(2.5) exposure has not been investigated. Thus, this study was aimed to investigate the protective effect of melatonin against PM(2.5)‐accelerated cardiac fibrosis. The echocardiography revealed that PM(2.5) had impaired both systolic and diastolic cardiac function in ApoE(−/−) mice. Histopathological analysis demonstrated that PM(2.5) induced cardiomyocyte hypertrophy and fibrosis, particularly perivascular fibrosis, while the melatonin administration was effective in alleviating PM(2.5)‐induced cardiac dysfunction and fibrosis in mice. Results of electron microscopy and confocal scanning laser microscope confirmed that melatonin had restorative effects against impaired mitochondrial ultrastructure and augmented mitochondrial ROS generation in PM(2.5)‐treated group. Further investigation revealed melatonin administration could significantly reverse the PM(2.5)‐induced phenotypic modulation of cardiac fibroblasts into myofibroblasts. For the first time, our study found that melatonin effectively alleviates PM(2.5)‐induced cardiac dysfunction and fibrosis via inhibiting mitochondrial oxidative injury and regulating SIRT3‐mediated SOD2 deacetylation. Our findings indicate that melatonin could be a therapy medicine for prevention and treatment of air pollution‐associated cardiac diseases.
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spelling pubmed-77572602020-12-28 Melatonin ameliorates PM(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis Jiang, Jinjin Liang, Shuang Zhang, Jingyi Du, Zhou Xu, Qing Duan, Junchao Sun, Zhiwei J Pineal Res Original Articles Fine particulate matter (PM(2.5)) exposure is correlated with the risk of developing cardiac fibrosis. Melatonin is a major secretory product of the pineal gland that has been reported to prevent fibrosis. However, whether melatonin affects the adverse health effects of PM(2.5) exposure has not been investigated. Thus, this study was aimed to investigate the protective effect of melatonin against PM(2.5)‐accelerated cardiac fibrosis. The echocardiography revealed that PM(2.5) had impaired both systolic and diastolic cardiac function in ApoE(−/−) mice. Histopathological analysis demonstrated that PM(2.5) induced cardiomyocyte hypertrophy and fibrosis, particularly perivascular fibrosis, while the melatonin administration was effective in alleviating PM(2.5)‐induced cardiac dysfunction and fibrosis in mice. Results of electron microscopy and confocal scanning laser microscope confirmed that melatonin had restorative effects against impaired mitochondrial ultrastructure and augmented mitochondrial ROS generation in PM(2.5)‐treated group. Further investigation revealed melatonin administration could significantly reverse the PM(2.5)‐induced phenotypic modulation of cardiac fibroblasts into myofibroblasts. For the first time, our study found that melatonin effectively alleviates PM(2.5)‐induced cardiac dysfunction and fibrosis via inhibiting mitochondrial oxidative injury and regulating SIRT3‐mediated SOD2 deacetylation. Our findings indicate that melatonin could be a therapy medicine for prevention and treatment of air pollution‐associated cardiac diseases. John Wiley and Sons Inc. 2020-11-16 2021-01 /pmc/articles/PMC7757260/ /pubmed/32730639 http://dx.doi.org/10.1111/jpi.12686 Text en © 2020 The Authors. Journal of Pineal Research published by John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Jiang, Jinjin
Liang, Shuang
Zhang, Jingyi
Du, Zhou
Xu, Qing
Duan, Junchao
Sun, Zhiwei
Melatonin ameliorates PM(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis
title Melatonin ameliorates PM(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis
title_full Melatonin ameliorates PM(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis
title_fullStr Melatonin ameliorates PM(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis
title_full_unstemmed Melatonin ameliorates PM(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis
title_short Melatonin ameliorates PM(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis
title_sort melatonin ameliorates pm(2.5)‐induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7757260/
https://www.ncbi.nlm.nih.gov/pubmed/32730639
http://dx.doi.org/10.1111/jpi.12686
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