Document Detail

Cardiovascular remodelling in coronary artery disease and heart failure.
MedLine Citation:
PMID:  24831770     Owner:  NLM     Status:  MEDLINE    
Remodelling is a response of the myocardium and vasculature to a range of potentially noxious haemodynamic, metabolic, and inflammatory stimuli. Remodelling is initially functional, compensatory, and adaptive but, when sustained, progresses to structural changes that become self-perpetuating and pathogenic. Remodelling involves responses not only of the cardiomyocytes, endothelium, and vascular smooth muscle cells, but also of interstitial cells and matrix. In this Review we characterise the remodelling processes in atherosclerosis, vascular and myocardial ischaemia-reperfusion injury, and heart failure, and we draw attention to potential avenues for innovative therapeutic approaches, including conditioning and metabolic strategies.
Gerd Heusch; Peter Libby; Bernard Gersh; Derek Yellon; Michael Böhm; Gary Lopaschuk; Lionel Opie
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2014-05-13
Journal Detail:
Title:  Lancet     Volume:  383     ISSN:  1474-547X     ISO Abbreviation:  Lancet     Publication Date:  2014 May 
Date Detail:
Created Date:  2014-06-02     Completed Date:  2014-06-10     Revised Date:  2014-11-05    
Medline Journal Info:
Nlm Unique ID:  2985213R     Medline TA:  Lancet     Country:  England    
Other Details:
Languages:  eng     Pagination:  1933-43     Citation Subset:  AIM; IM    
Copyright Information:
Copyright © 2014 Elsevier Ltd. All rights reserved.
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MeSH Terms
Adaptation, Physiological / physiology*
Coronary Artery Disease / physiopathology*
Coronary Vessels / physiopathology
Heart Failure / physiopathology*
Ischemic Preconditioning, Myocardial / methods
Mitochondria, Heart / metabolism
Myocardial Reperfusion Injury / physiopathology
Ventricular Remodeling / physiology
Grant Support
NF-SI-0510-10164//Department of Health; R01 HL080472/HL/NHLBI NIH HHS; RG/08/015/26411//British Heart Foundation

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