Document Detail


Molecular mechanisms that control interstitial fibrosis in the pressure-overloaded heart.
MedLine Citation:
PMID:  20880837     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
When considering the pathological steps in the progression from cardiac overload towards the full clinical syndrome of heart failure, it is becoming increasingly clear that the extracellular matrix (ECM) is an important determinant in this process. Chronic pressure overload induces a number of structural alterations, not only hypertrophy of cardiomyocytes but also an increase in ECM proteins in the interstitium and perivascular regions of the myocardium. When this culminates in excessive fibrosis, myocardial compliance decreases and electrical conduction is affected. Altogether, fibrosis is associated with an increased risk of ventricular dysfunction and arrhythmias. Consequently, anti-fibrotic strategies are increasingly recognized as a promising approach in the prevention and treatment of heart failure. Thus, dissecting the molecular mechanisms underlying the development of cardiac fibrosis is of great scientific and therapeutic interest. In this review, we provide an overview of the available evidence supporting the general idea that fibrosis plays a causal role in deteriorating cardiac function. Next, we will delineate the signalling pathways importantly governed by transforming growth factor β (TGFβ) in the control of cardiac fibrosis. Finally, we will discuss the recent discovery that miRNAs importantly regulate cardiac fibrosis.
Authors:
Esther E Creemers; Yigal M Pinto
Related Documents :
22044707 - Update on the medical treatment of stable angina.
18158477 - Systolic heart failure: chronic and acute syndromes.
3552317 - Calcium-channel blockade in the management of severe chronic congestive heart failure: ...
16283977 - Nontransplant surgical alternatives for heart failure.
10498147 - Relation between infarct artery patency at late angiography after acute myocardial infa...
23953387 - What is the optimum adjunctive reperfusion strategy for primary percutaneous coronary i...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-28
Journal Detail:
Title:  Cardiovascular research     Volume:  89     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-01-13     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  265-72     Citation Subset:  IM    
Affiliation:
Heart Failure Research Center, Academic Medical Center, Meibergdreef 15, Room L2-108-3, 1105 AZ Amsterdam, The Netherlands. e.e.creemers@amc.uva.nl
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Disrupted-in-schizophrenia 1 (DISC1) plays essential roles in mitochondria in collaboration with Mit...
Next Document:  Cdc37-Hsp90 complexes are responsive to nucleotide-induced conformational changes and binding of fur...