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NOX family members normally regulate cellular physiological functions, but under abnormal circumstances contribute to the pathogenesis of cell/tissue damage associated with infections and vascular disorders (Panday et al., 2015)
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Unlike mitochondrial fission, pharmacological activation of mitophagy is associated with angiotensin II and atrial natriuretic peptide levels, reducing cardiomyocyte apoptosis and myocardial fibrosis in a model of pressure overload-induced chronic cardiac insufficiency [75]
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