期刊
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
卷 88, 期 1, 页码 1-8出版社
CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
DOI: 10.1139/Y09-092
关键词
intracellular signaling; peptides and proteins; protein kinases; RhoA/Rho-kinase pathway; muscle; smooth; vascular; pulmonary hypertension; pulmonary vascular bed; systemic vascular bed; signal transduction; inhibitors/pharmacology; cardiovascular diseases; fasudil; HA-1077; Y-27632
资金
- NIH [HL62000, HL77421, ES10018, RR16456]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR016456] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL077421, R01HL062000] Funding Source: NIH RePORTER
Calcium is the major intracellular messenger that triggers smooth muscle contraction. The study of calcium-binding proteins, such as calmodulin and its downstream effectors, reveals critical regulation of smooth muscle Contraction by protein kinases and phosphatases. Moreover, the small GTP-binding protein RhoA and its downstream effector protein, Rho-kinase, have been shown to play a novel role in the regulation of smooth muscle contraction. Studies have shown that the activation of Rho-kinase is involved in the development of endothelial dysfunction, inflammation, restenosis, and increased vascular tone in a number of cardiovascular disorders. Because inhibitors of this pathway promote vasodilation independent of the mechanism that increases vasoconstrictor tone, it is our hypothesis that Rho-kinase is constitutively active in regulating vasoconstrictor tone in the pulmonary and systemic vascular beds. Studies in the literature suggest that the RhoA/Rho-kinase pathway has an important role in the pathogenesis of pulmonary hypertension.
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