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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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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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. |
format | Online Article Text |
id | pubmed-7757260 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
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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