Document Detail


Angiotensin II and oxidative stress in the failing heart.
MedLine Citation:
PMID:  22429089     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
SIGNIFICANCE: Despite recent medical advances, cardiovascular disease and heart failure (HF) continue to be major health concerns, and related mortality remains high. As a result, investigation of the mechanisms involved in the development of HF continues to be an active field of study.
RECENT ADVANCES: The renin-angiotensin system (RAS) and its effector molecule, angiotensin (Ang) II, affect cardiac function through both systemic and local actions, and have been shown to play a major role in cardiac remodeling and dysfunction in the failing heart. Many of the downstream effects of AngII signaling are mediated by elevated levels of reactive oxygen species (ROS) and oxidative stress, which have also been implicated in the pathology of HF.
CRITICAL ISSUES: Inhibitors of the RAS have proven beneficial in the treatment of patients at risk for and suffering from HF, but remain only partially effective. ROS can be generated from several different sources, and the oxidative state is normally tightly regulated in the heart. How AngII increases ROS levels and causes dysregulation of the cardiac oxidative state has been the subject of considerable interest in recent years.
FUTURE DIRECTIONS: A better understanding of this process and the mechanisms involved should lead to the development of more effective HF therapies and improved outcomes.
Authors:
Daniela Zablocki; Junichi Sadoshima
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2012-05-03
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  19     ISSN:  1557-7716     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2013 Oct 
Date Detail:
Created Date:  2013-09-13     Completed Date:  2014-03-25     Revised Date:  2014-10-19    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1095-109     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / metabolism*,  physiology
Animals
Cardiovascular Diseases / metabolism*,  physiopathology,  therapy
Heart Failure / metabolism*,  physiopathology,  therapy
Humans
Mitochondria / metabolism*,  pathology
NADPH Oxidase / metabolism
Oxidative Stress / genetics
Reactive Oxygen Species / metabolism*
Renin-Angiotensin System
Grant Support
ID/Acronym/Agency:
AG27211/AG/NIA NIH HHS; HL102738/HL/NHLBI NIH HHS; HL59139/HL/NHLBI NIH HHS; HL67724/HL/NHLBI NIH HHS; HL69020/HL/NHLBI NIH HHS; HL91469/HL/NHLBI NIH HHS; R01 AG023039/AG/NIA NIH HHS; R01 HL067724/HL/NHLBI NIH HHS; R01 HL091469/HL/NHLBI NIH HHS; R01 HL102738/HL/NHLBI NIH HHS; R01 HL112330/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 11128-99-7/Angiotensin II; EC 1.6.3.1/NADPH Oxidase
Comments/Corrections

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