Key result
Natural antioxidants protect against cardiac remodeling and contractile dysfunction by reducing reactive oxygen species.
This review highlights the mechanistic role of reactive oxygen species in cardiac pathogenesis and the potential therapeutic benefits of natural antioxidants.
Should not yet change practice for cardiac remodeling; leaves open clinical translation of natural antioxidants pending randomized trials.
Homeostasis in the level of reactive oxygen species (ROS) in cardiac myocytes plays a critical role in regulating their physiological functions. Disturbance of balance between generation and removal of ROS is a major cause of cardiac myocyte remodeling, dysfunction, and failure. Cardiac myocytes possess several ROS-producing pathways, such as mitochondrial electron transport chain, NADPH oxidases, and nitric oxide synthases, and have endogenous antioxidation mechanisms. Cardiac Ca2+-signaling toolkit proteins, as well as mitochondrial functions, are largely modulated by ROS under physiological and pathological conditions, thereby producing alterations in contraction, membrane conductivity, cell metabolism and cell growth and death. Mechanical stresses under hypertension, post-myocardial infarction, heart failure, and valve diseases are the main causes for stress-induced cardiac remodeling and functional failure, which are associated with ROS-induced pathogenesis. Experimental evidence demonstrates that many cardioprotective natural antioxidants, enriched in foods or herbs, exert beneficial effects on cardiac functions (Ca2+ signal, contractility and rhythm), myocytes remodeling, inflammation and death in pathological hearts. The review may provide knowledge and insight into the modulation of cardiac pathogenesis by ROS and natural antioxidants.
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Woo et al. (2021) conducted a review in Cardiac pathogenesis, heart failure, and arrhythmias. Natural antioxidants was evaluated. Natural antioxidants, such as flavonoids and resveratrol, exert cardioprotective effects by modulating reactive oxygen species, thereby preventing cardiac remodeling, contractile dysfunction, and apoptosis.
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