The role of RhoA/Rho kinase pathway in endothelial dysfunction

Research output: Contribution to journalReview article

37 Citations (Scopus)

Abstract

Endothelial dysfunction is a key event in the development of vascular disease, and it precedes clinically obvious vascular pathology. Abnormal activation of the RhoA/Rho kinase (ROCK) pathway has been found to elevate vascular tone through unbalancing the production of vasodilating and vasoconstricting substances. Inhibition of the RhoA/ROCK pathway can prevent endothelial dysfunction in a variety of pathological conditions. This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of the ROCK pathway and its roles in endothelial dysfunction.

Original languageEnglish (US)
Pages (from-to)165-170
Number of pages6
JournalJournal of Cardiovascular Disease Research
Volume1
Issue number4
DOIs
StatePublished - Jan 1 2010

Fingerprint

rho-Associated Kinases
Blood Vessels
Vascular Diseases
Pathology

Keywords

  • Endothelial dysfunction
  • Rho kinase
  • endothelium-dependent contractions
  • nitric oxide

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

@article{fa916154c20b4044bff09699000b3616,
title = "The role of RhoA/Rho kinase pathway in endothelial dysfunction",
abstract = "Endothelial dysfunction is a key event in the development of vascular disease, and it precedes clinically obvious vascular pathology. Abnormal activation of the RhoA/Rho kinase (ROCK) pathway has been found to elevate vascular tone through unbalancing the production of vasodilating and vasoconstricting substances. Inhibition of the RhoA/ROCK pathway can prevent endothelial dysfunction in a variety of pathological conditions. This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of the ROCK pathway and its roles in endothelial dysfunction.",
keywords = "Endothelial dysfunction, Rho kinase, endothelium-dependent contractions, nitric oxide",
author = "Lin Yao and {Romero Lucas}, {Maritza Josefina} and {Flores Toque}, {Haroldo Alfredo} and Guang Yang and Caldwell, {Ruth B} and Caldwell, {Robert William}",
year = "2010",
month = "1",
day = "1",
doi = "10.4103/0975-3583.74258",
language = "English (US)",
volume = "1",
pages = "165--170",
journal = "Journal of Cardiovascular Disease Research",
issn = "0975-3583",
publisher = "Medknow Publications and Media Pvt. Ltd",
number = "4",

}

TY - JOUR

T1 - The role of RhoA/Rho kinase pathway in endothelial dysfunction

AU - Yao, Lin

AU - Romero Lucas, Maritza Josefina

AU - Flores Toque, Haroldo Alfredo

AU - Yang, Guang

AU - Caldwell, Ruth B

AU - Caldwell, Robert William

PY - 2010/1/1

Y1 - 2010/1/1

N2 - Endothelial dysfunction is a key event in the development of vascular disease, and it precedes clinically obvious vascular pathology. Abnormal activation of the RhoA/Rho kinase (ROCK) pathway has been found to elevate vascular tone through unbalancing the production of vasodilating and vasoconstricting substances. Inhibition of the RhoA/ROCK pathway can prevent endothelial dysfunction in a variety of pathological conditions. This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of the ROCK pathway and its roles in endothelial dysfunction.

AB - Endothelial dysfunction is a key event in the development of vascular disease, and it precedes clinically obvious vascular pathology. Abnormal activation of the RhoA/Rho kinase (ROCK) pathway has been found to elevate vascular tone through unbalancing the production of vasodilating and vasoconstricting substances. Inhibition of the RhoA/ROCK pathway can prevent endothelial dysfunction in a variety of pathological conditions. This review, based on recent molecular, cellular, and animal studies, focuses on the current understanding of the ROCK pathway and its roles in endothelial dysfunction.

KW - Endothelial dysfunction

KW - Rho kinase

KW - endothelium-dependent contractions

KW - nitric oxide

UR - http://www.scopus.com/inward/record.url?scp=79952937372&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79952937372&partnerID=8YFLogxK

U2 - 10.4103/0975-3583.74258

DO - 10.4103/0975-3583.74258

M3 - Review article

C2 - 21264179

AN - SCOPUS:79952937372

VL - 1

SP - 165

EP - 170

JO - Journal of Cardiovascular Disease Research

JF - Journal of Cardiovascular Disease Research

SN - 0975-3583

IS - 4

ER -