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Am J Physiol Cell Physiol 290: C661-C668, 2006; doi:10.1152/ajpcell.00459.2005
0363-6143/06 $8.00
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INVITED REVIEW

Physiological role of ROCKs in the cardiovascular system

Kensuke Noma, Naotsugu Oyama, and James K. Liao

Vascular Medicine Research Unit, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts

Rho-associated kinases (ROCKs), the immediate downstream targets of RhoA, are ubiquitously expressed serine-threonine protein kinases that are involved in diverse cellular functions, including smooth muscle contraction, actin cytoskeleton organization, cell adhesion and motility, and gene expression. Recent studies have shown that ROCKs may play a pivotal role in cardiovascular diseases such as vasospastic angina, ischemic stroke, and heart failure. Indeed, inhibition of ROCKs by statins or other selective inhibitors leads to the upregulation and activation of endothelial nitric oxide synthase (eNOS) and reduction of vascular inflammation and atherosclerosis. Thus inhibition of ROCKs may contribute to some of the cholesterol-independent beneficial effects of statin therapy. Currently, two ROCK isoforms have been identified, ROCK1 and ROCK2. Because ROCK inhibitors are nonselective with respect to ROCK1 and ROCK2 and also, in some cases, may be nonspecific with respect to other ROCK-related kinases such as myristolated alanine-rich C kinase substrate (MARCKS), protein kinase A, and protein kinase C, the precise role of ROCKs in cardiovascular disease remains unknown. However, with the recent development of ROCK1- and ROCK2-knockout mice, further dissection of ROCK signaling pathways is now possible. Herein we review what is known about the physiological role of ROCKs in the cardiovascular system and speculate about how inhibition of ROCKs could provide cardiovascular benefits.

Rho GTPase; Rho-kinase; vascular endothelium; contraction; actin cytoskeleton; nitric oxide; statins



Address for reprint requests and other correspondence: J. K. Liao, Brigham & Women's Hospital, 65 Landsdowne St., Rm. 275, Cambridge, MA (e-mail: jliao{at}rics.bwh.harvard.edu)




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