期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 10, 期 6, 页码 1045-1059出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2007.1986
关键词
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资金
- NHLBI NIH HHS [R01 HL038206-18, P01 HL058000-090001, HL58000, HL38206, HL058863, P01 HL058000, R01 HL058863-10, R01 HL058863, P01 HL075209-04, HL075209, P01 HL075209, R01 HL038206] Funding Source: Medline
Accumulating evidence supports the importance of redox signaling in the pathogenesis and progression of hypertension. Redox signaling is implicated in many different physiological and pathological processes in the vasculature. High blood pressure is in part determined by elevated total peripheral vascular resistance, which is ascribed to dysregulation of vasomotor function and structural remodeling of blood vessels. Aberrant redox signaling, usually induced by excessive production of reactive oxygen species (ROS) and/or by decreases in antioxidant activity, can induce alteration of vascular function. ROS increase vascular tone by influencing the regulatory role of endothelium and by direct effects on the contractility of vascular smooth muscle. ROS contribute to vascular remodeling by influencing phenotype modulation of vascular smooth muscle cells, aberrant growth and death of vascular cells, cell migration, and extracellular matrix (ECM) reorganization. Thus, there are diverse roles of the vascular redox system in hypertension, suggesting that the complexity of redox signaling in distinct spatial spectrums should be considered for a better understanding of hypertension.
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