Document Detail


Extracellular matrix and fibroblast communication following myocardial infarction.
MedLine Citation:
PMID:  22926488     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The extracellular matrix (ECM) provides structural support by serving as a scaffold for cells, and as such the ECM maintains normal tissue homeostasis and mediates the repair response following injury. In response to myocardial infarction (MI), ECM expression is generally upregulated in the left ventricle (LV), which regulates LV remodeling by modulating scar formation. The ECM directly affects scar formation by regulating growth factor release and cell adhesion and indirectly affects scar formation by regulating the inflammatory, angiogenic, and fibroblast responses. This review summarizes the current literature on ECM expression patterns and fibroblast mechanisms in the myocardium, focusing on the ECM response to MI. In addition, we discuss future research areas that are needed to better understand the molecular mechanisms of ECM action, both in general and as a means to optimize infarct healing.
Authors:
Yonggang Ma; Ganesh V Halade; Merry L Lindsey
Related Documents :
20410148 - Medical treatment of mural left ventricular endocarditis mass: a case report.
1200038 - Unusual echographic manifestations of right and left heart myxomas.
3178348 - Surgical removal of a mobile, pedunculated left ventricular thrombus: report of 4 cases.
18583288 - Surgical resection of left atrial myxoma presenting with acute multiple hemorrhagic cer...
1688988 - Calcium dobesilate (cls 2210) protects the myocardium in early acute myocardial infarct...
3416328 - Lymphocyte potassium and magnesium concentrations as prognostic factors after acute myo...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review     Date:  2012-08-28
Journal Detail:
Title:  Journal of cardiovascular translational research     Volume:  5     ISSN:  1937-5395     ISO Abbreviation:  J Cardiovasc Transl Res     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-11     Completed Date:  2013-05-21     Revised Date:  2014-06-11    
Medline Journal Info:
Nlm Unique ID:  101468585     Medline TA:  J Cardiovasc Transl Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  848-57     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
CCN Intercellular Signaling Proteins / metabolism
Cell-Matrix Junctions / metabolism*,  pathology
Cicatrix / metabolism,  pathology
Extracellular Matrix / metabolism*,  pathology
Fibroblasts / metabolism*,  pathology
Humans
Myocardial Infarction / metabolism*,  pathology
Myocardium / metabolism*,  pathology
Signal Transduction*
Grant Support
ID/Acronym/Agency:
1K99AT006704-01/AT/NCCAM NIH HHS; HHSN268201000036C/HL/NHLBI NIH HHS; HHSN268201000036C (N01-HV-00244)/HV/NHLBI NIH HHS; K99 AT006704/AT/NCCAM NIH HHS; R00 AT006704/AT/NCCAM NIH HHS; R01 HL075360/HL/NHLBI NIH HHS; R01 HL075360/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/CCN Intercellular Signaling Proteins
Comments/Corrections

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


Previous Document:  Expression patterns of emmprin and monocarboxylate transporter-1 in ovarian epithelial tumors.
Next Document:  Do fluoroscopy and postoperative radiographs correlate for periacetabular osteotomy corrections?