title: Redox regulation of endothelial cell fate.
abstract: Endothelial cells (ECs) are present throughout blood vessels and have variable roles in both physiological and pathological settings. EC fate is altered and regulated by several key factors in physiological or pathological conditions. Reactive nitrogen species and reactive oxygen species derived from NAD(P)H oxidases, mitochondria, or nitric oxide-producing enzymes are not only cytotoxic but also compose a signaling network in the redox system. The formation, actions, key molecular interactions, and physiological and pathological relevance of redox signals in ECs remain unclear. We review the identities, sources, and biological actions of oxidants and reductants produced during EC function or dysfunction. Further, we discuss how ECs shape key redox sensors and examine the biological functions, transcriptional responses, and post-translational modifications evoked by the redox system in ECs. We summarize recent findings regarding the mechanisms by which redox signals regulate the fate of ECs and address the outcome of altered EC fate in health and disease. Future studies will examine if the redox biology of ECs can be targeted in pathophysiological conditions.
authors.affiliation: Section of Molecular Medicine, Department of Internal Medicine, University of Oklahoma Health Sciences Center, 941 Stanton L Young Blvd., Oklahoma City, OK, 73104, USA, ping-song@ouhsc.edu.
authors.forename: Ping
authors.initials: P
authors.lastname: Song
authors.forename: Ming-Hui
authors.initials: MH
authors.lastname: Zou
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D002318:Cardiovascular Diseases / Q000378:metabolism / Q000473:pathology; D002453:Cell Cycle / Q000502:physiology; D002465:Cell Movement; D054338:Cell Transdifferentiation; D003545:Cysteine / Q000737:chemistry; D003920:Diabetes Mellitus / Q000378:metabolism / Q000473:pathology; D042783:Endothelial Cells / Q000166:cytology* / Q000378:metabolism; D051858:Forkhead Transcription Factors / Q000502:physiology; D006801:Humans; D006862:Hydrogen Sulfide / Q000378:metabolism; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D008954:Models, Biological; D051267:NF-E2-Related Factor 2 / Q000502:physiology; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology; D018919:Neovascularization, Physiologic; D009569:Nitric Oxide / Q000502:physiology; D009765:Obesity / Q000378:metabolism / Q000473:pathology; D010084:Oxidation-Reduction; D010088:Oxidoreductases / Q000502:physiology; D026361:Reactive Nitrogen Species / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D051858:Forkhead Transcription Factors; D051267:NF-E2-Related Factor 2; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D010088:Oxidoreductases; D003545:Cysteine; D006862:Hydrogen Sulfide