Open AccessInterplay Between Reactive Oxygen/Reactive Nitrogen Species and Metabolism in Vascular Biology and Disease
Author(s) -
Masuko UshioFukai,
Dipankar Ash,
Sheela Nagarkoti,
Eric J. Belin de Chantemèle,
David Fulton,
Tohru Fukai
Publication year - 2021
Publication title -
antioxidants and redox signaling
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.277
H-Index - 190
eISSN - 1557-7716
pISSN - 1523-0864
DOI - 10.1089/ars.2020.8161
Subject(s) - reactive oxygen species , pentose phosphate pathway , reactive nitrogen species , nicotinamide adenine dinucleotide phosphate , metabolic pathway , glycolysis , microbiology and biotechnology , biochemistry , oxidative phosphorylation , signal transduction , biology , nitric oxide , chemistry , metabolism , enzyme , oxidase test , endocrinology
Reactive oxygen species (ROS; e.g ., superoxide [O 2 •- ] and hydrogen peroxide [H 2 O 2 ]) and reactive nitrogen species (RNS; e.g ., nitric oxide [NO • ]) at the physiological level function as signaling molecules that mediate many biological responses, including cell proliferation, migration, differentiation, and gene expression. By contrast, excess ROS/RNS, a consequence of dysregulated redox homeostasis, is a hallmark of cardiovascular disease. Accumulating evidence suggests that both ROS and RNS regulate various metabolic pathways and enzymes. Recent studies indicate that cells have mechanisms that fine-tune ROS/RNS levels by tight regulation of metabolic pathways, such as glycolysis and oxidative phosphorylation. The ROS/RNS-mediated inhibition of glycolytic pathways promotes metabolic reprogramming away from glycolytic flux toward the oxidative pentose phosphate pathway to generate nicotinamide adenine dinucleotide phosphate (NADPH) for antioxidant defense. This review summarizes our current knowledge of the mechanisms by which ROS/RNS regulate metabolic enzymes and cellular metabolism and how cellular metabolism influences redox homeostasis and the pathogenesis of disease. A full understanding of these mechanisms will be important for the development of new therapeutic strategies to treat diseases associated with dysregulated redox homeostasis and metabolism. Antioxid. Redox Signal . 34, 1319-1354.