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PMID: 15090271 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S. Review

Redox regulation of angiotensin II signaling in the heart.

Journal of cellular and molecular medicine ·Vol. 8 ·No. 1 ·2004-00-00 ·Pages 144-52

Das DK, Maulik N, Engelman RM

Abstract

A large number of studies have demonstrated the role of angiotensin II in cardiac preconditioning against ischemic reperfusion injury. Generally, angiotensin II is a detrimental factor for the heart, and its inhibition with an ACE inhibitor provides cardioprotection. This review provides an explanation for such paradoxical behavior of angiotensin II. Angiotensin II can potentiate the induction of the expression of a variety of redox-sensitive factors including p38 MAPK, JNK and Akt, IGF-IR, EGF-R, and HO-1 as well as redox-regulated genes and transcription factors such as NFkappaB. It becomes increasingly apparent that during the earlier phase, the heart attempts to adapt itself against the detrimental effects of angiotensin II by upregulating several cardioprotective genes and proteins. These genes and proteins are redox-regulated and the antioxidants or ROS scavengers block their expressions. Interestingly, an identical pattern of cardioprotective proteins and genes are expressed in the preconditioned heart, which are also inhibited with ROS scavengers. It is tempting to speculate that the induction of the expression of the redox-sensitive cardioprotective proteins is the results of adaptation of the heart against the oxidative stress resulting from angiotensin II; and preconditioning is the net result of harnessing its own protection during ischemic and/or oxidative stress through its ability to trigger redox signaling.

MeSH Terms
Angiotensin II/metabolism Animals Heart/physiology Humans Ischemic Preconditioning, Myocardial Models, Biological Myocardium/metabolism Oxidation-Reduction Oxidative Stress Reactive Oxygen Species Signal Transduction
Chemicals
Reactive Oxygen Species Angiotensin II
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Das Dipak K
Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut 06030-1110, USA. [email protected]
Maulik Nilanjana
Engelman Richard M
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Article Info
Journal
Journal of cellular and molecular medicine
Abbr.
J Cell Mol Med
ISSN
1582-1838
DOI
10.1111/j.1582-4934.2004.tb00270.x
Email
[email protected]
Published
2004-00-00
Pages
144-52
Language
English
Region
England
NLM ID
101083777
PMCID
PMC6740106
Subset
IM
Grants
NHLBI NIH HHS · HL 22559 · United States
NHLBI NIH HHS · HL 33889 · United States
NHLBI NIH HHS · HL 56803 · United States
NHLBI NIH HHS · HL 63317 · United States
NHLBI NIH HHS · HL 69910 · United States
External Links
PubMed source DOI: 10.1111/j.1582-4934.2004.tb00270.x PMC Full Text View journal details
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