Diabetes and Cardiovascular Center, Harry S. Truman VA Medical Center, Columbia, MO, USA.
Rev Cardiovasc Med. 2011;12(1):21-9. doi: 10.3909/ricm0555.
Loss of reduction-oxidation (redox) homeostasis and generation of excess free oxygen radicals play an important role in the pathogenesis of diabetes, hypertension, and consequent cardiovascular disease. Reactive oxygen species are integral in routine in physiologic mechanisms. However, loss of redox homeostasis contributes to proinflammatory and profibrotic pathways that promote impairments in insulin metabolic signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular and renal structural and functional abnormalities. Redox control of metabolic function is a dynamic process with reversible pro- and anti-free radical processes. Labile iron is necessary for the catalysis of superoxide anion, hydrogen peroxide, and the generation of the damaging hydroxyl radical. Acute hypoxia and cellular damage in cardiovascular tissue liberate larger amounts of cytosolic and extracellular iron that is poorly liganded; thus, large increases in the generation of oxygen free radicals are possible, causing tissue damage. The understanding of iron and the imbalance of redox homeostasis within the vasculature is integral in hypertension and progression of metabolic dysregulation that contributes to insulin resistance, endothelial dysfunction, and cardiovascular and kidney disease.
氧化还原（redox）稳态的丧失和过量游离氧自由基的产生在糖尿病、高血压以及随之而来的心血管疾病的发病机制中起着重要作用。活性氧自由基是生理机制中不可或缺的一部分。然而，氧化还原稳态的丧失会导致促炎和促纤维化途径，从而损害胰岛素代谢信号转导、内皮介导的血管舒张，并导致相关的心血管和肾脏结构和功能异常。代谢功能的氧化还原控制是一个动态过程，具有可逆的促自由基和抗自由基过程。不稳定的铁是超氧阴离子、过氧化氢和有害羟自由基生成的催化所必需的。心血管组织中的急性缺氧和细胞损伤会释放出大量结合不良的胞质和细胞外铁；因此，氧自由基的大量生成是可能的，会导致组织损伤。理解铁和血管内氧化还原稳态的失衡对于高血压以及代谢失调的进展至关重要，代谢失调会导致胰岛素抵抗、内皮功能障碍以及心血管和肾脏疾病。
