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- W1534181195 abstract "Heme oxygenase-1 (HO-1) catalyzes the oxidative degradation of heme to carbon monoxide (CO), iron, and biliverdin. Biliverdin is promptly metabolized to bilirubin by biliverdin reductase while iron is rapidly chelated by ferritin or excreted and recycled for heme synthesis. Clinical and experimental studies indicate that HO-1 is induced in atherosclerotic lesions and that it functions in an adaptive manner to limit plaque size and vulnerability. The anti-atherogenic actions of HO-1 are largely mediated by its reaction products, CO and the bile pigments biliverdin and bilirubin. These heme metabolites exert potent antioxidant, anti-inflammatory, anti-thrombotic, anti-apoptotic, and vasodilatory effects in the circulation. In addition, CO and the bile pigments act in concert to maintain homeostatic balance at sites of arterial damage by regulating the proliferation, migration, activation, maturation, differentiation, and/or infiltration of vascular cells, platelets, and immune cells. Moreover, HO-1 promotes vascular function by preserving endothelial nitric oxide synthase and soluble guanylate cyclase expression and vascular repair by mobilizing and recruiting endothelial progenitor cells to arterial lesions. This chapter will discuss the regulation of HO-1 expression in vascular lesions and highlight potential mechanisms by which HO-1 suppresses atherosclerosis, focusing on the cellular and molecular actions of CO and bilirubin. In addition, it will describe potential therapeutic strategies targeting HO-1 and its reaction products in preventing the development and progression of atherosclerosis." @default.
- W1534181195 created "2016-06-24" @default.
- W1534181195 creator A5070064210 @default.
- W1534181195 date "2015-03-27" @default.
- W1534181195 modified "2023-09-26" @default.
- W1534181195 title "Protective Role of Heme Oxygenase‐1 in Atherosclerosis" @default.
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- W1534181195 doi "https://doi.org/10.1002/9781118828533.ch29" @default.
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