Narayana Anilkumar

TL;DR: H2O2 formation is an intrinsic property of Nox4 that involves its E- loop, and the structure of the E-loop may hinder O2̇̄ egress and/or provide a source for protons, allowing dismutation to form H1O2.

TL;DR: Data indicate that cardiomyocyte Nox4 is a unique inducible regulator of myocardial angiogenesis, a key determinant of cardiac adaptation to overload stress, and has wider relevance to the use of nonspecific antioxidant approaches in cardiac disease.

TL;DR: These are the main redox-regulated pathways that are involved in cardiac myocyte excitation–contraction coupling, differentiation, hypertrophy, and stress responses and the particular pathways and processes that they affect are reviewed.

TL;DR: Endothelial Nox4 exerts potentially beneficial effects on vasodilator function and blood pressure that are attributable to H2O2 production, which contrast markedly with those reported for Nox1 and Nox2, which involve superoxide-mediated inactivation of nitric oxide.

TL;DR: The data suggest that the Nox2-containing reduced nicotinamide-adenine dinucleotide phosphate oxidase contributes significantly to the processes underlying adverse cardiac remodeling and contractile dysfunction post-MI.