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Published on: April 16, 2018
Melatonin ameliorates PM2.5 -induced cardiac perivascular fibrosis through regulating mitochondrial redox homeostasis
Jinjin Jiang1,2, Shuang Liang1,2, Jingyi Zhang1,2
1Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing, China.
Abstract:
Fine particulate matter (PM2.5 ) 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 PM2.5 exposure has not been investigated. Thus, this study was aimed to investigate the protective effect of melatonin against PM2.5 -accelerated cardiac fibrosis. The echocardiography revealed that PM2.5 had impaired both systolic and diastolic cardiac function in ApoE-/- mice. Histopathological analysis demonstrated that PM2.5 induced cardiomyocyte hypertrophy and fibrosis, particularly perivascular fibrosis, while the melatonin administration was effective in alleviating PM2.5 -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 PM2.5 -treated group. Further investigation revealed melatonin administration could significantly reverse the PM2.5 -induced phenotypic modulation of cardiac fibroblasts into myofibroblasts. For the first time, our study found that melatonin effectively alleviates PM2.5 -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.
Insights
Melatonin protects against heart damage caused by fine particulate matter (PM2.5) exposure. This study shows melatonin reduces PM2.5-induced cardiac fibrosis and dysfunction by protecting mitochondria.
Area of Science:
- Environmental Health
- Cardiovascular Biology
- Endocrinology
Background:
- Fine particulate matter (PM2.5) exposure is linked to increased cardiac fibrosis risk.
- Melatonin, a pineal gland hormone, is known to possess anti-fibrotic properties.
- The impact of melatonin on PM2.5-induced cardiac effects remains uninvestigated.
Purpose of the Study:
- To investigate the protective potential of melatonin against PM2.5-accelerated cardiac fibrosis.
- To elucidate the mechanisms underlying melatonin's effects on PM2.5-induced cardiac damage.
Main Methods:
- Utilized ApoE-/- mice exposed to PM2.5, with and without melatonin administration.
- Performed echocardiography for cardiac function assessment.
- Conducted histopathological analysis, electron microscopy, and confocal microscopy.
Main Results:
- PM2.5 exposure impaired cardiac function and induced cardiomyocyte hypertrophy and fibrosis in mice.
- Melatonin administration alleviated PM2.5-induced cardiac dysfunction and fibrosis.
- Melatonin restored mitochondrial ultrastructure, reduced mitochondrial ROS, and inhibited fibroblast-myofibroblast transition.
Conclusions:
- Melatonin effectively mitigates PM2.5-induced cardiac dysfunction and fibrosis.
- The protective effect involves inhibiting mitochondrial oxidative injury and regulating SIRT3-mediated SOD2 deacetylation.
- Melatonin shows promise as a therapeutic agent for air pollution-related cardiac diseases.
