Oxidative stress pathway in cardiomyocytes (OS pathway)

The oxidative stress pathway in cardiomyocytes is a complex biochemical network characterized by the production, regulation, and deleterious effects of reactive oxygen species (ROS) and reactive nitrogen species (RNS) within the heart muscle [1, 11]. In a healthy state, low levels of ROS, primarily generated by mitochondria and NADPH oxidases (NOX), serve as essential signaling molecules for cardiomyocyte differentiation, growth, and excitation-contraction coupling [6, 11, 15]. However, pathological conditions such as myocardial infarction, heart failure, and diabetic cardiomyopathy trigger an overproduction of ROS from sources like dysfunctional mitochondria, xanthine oxidase, and uncoupled nitric oxide synthase [4, 7, 13]. This excess leads to oxidative damage of critical cellular components, including lipids (lipid peroxidation), proteins (carbonylation), and DNA, which subsequently activates pro-apoptotic signaling (e.g., p53, caspases) and promotes cardiac fibrosis and remodeling [1, 2, 5, 10]. Therapeutic interventions target this pathway by either inhibiting ROS-generating enzymes or bolstering endogenous antioxidant defenses, such as the Nrf2-mediated response, to mitigate myocardial injury and preserve cardiac function [10, 12, 16].

Other names

Redox signaling pathway in cardiomyocytesMyocardial oxidative stress pathwayCardiac redox signalingROS signaling in cardiomyocytesOxidative stress in cardiomyocytes

Inhibition of reactive oxygen species (ROS) production (e.g., NOX inhibition, xanthine oxidase inhibition); scavenging of free radicals; activation of endogenous antioxidant defense systems (e.g., Nrf2 activation); protection of mitochondrial function and reduction of mitochondrial ROS leakage.