Section of Molecular Medicine, Department of Internal Medicine, University of Oklahoma Health Sciences Center, 941 Stanton L Young Blvd., Oklahoma City, OK, 73104, USA,
Cell Mol Life Sci. 2014 Sep;71(17):3219-39. doi: 10.1007/s00018-014-1598-z. Epub 2014 Mar 15.
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.
内皮细胞（ECs）存在于血管的各个部位，在生理和病理环境中具有不同的作用。在生理或病理条件下，内皮细胞的命运受到几种关键因子的改变和调节。来自 NAD（P）H 氧化酶、线粒体或产生一氧化氮的酶的活性氮和活性氧不仅具有细胞毒性，而且在氧化还原系统中构成信号网络。内皮细胞中氧化还原信号的形成、作用、关键分子相互作用以及生理和病理相关性尚不清楚。我们回顾了在 EC 功能或功能障碍期间产生的氧化剂和还原剂的身份、来源和生物学作用。此外，我们讨论了 EC 如何塑造关键的氧化还原传感器，并研究了氧化还原系统在 EC 中引发的生物学功能、转录反应和翻译后修饰。我们总结了关于氧化还原信号调节 EC 命运的机制的最新发现，并探讨了改变的 EC 命运在健康和疾病中的结果。未来的研究将探讨是否可以针对病理生理条件下 EC 的氧化还原生物学进行靶向治疗。
