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Integrins, focal adhesions, and cardiac fibroblasts

Authors
 Ana Maria Manso  ;  Seok-Min Kang  ;  Robert S. Ross 
Citation
 JOURNAL OF INVESTIGATIVE MEDICINE, Vol.57(8) : 856-860, 2009 
Journal Title
JOURNAL OF INVESTIGATIVE MEDICINE
ISSN
 1081-5589 
Issue Date
2009
MeSH
Animals ; Fibroblasts/pathology ; Fibroblasts/physiology* ; Focal Adhesions/genetics ; Focal Adhesions/metabolism* ; Focal Adhesions/pathology ; Humans ; Integrins/genetics ; Integrins/physiology* ; Myocytes, Cardiac/pathology ; Myocytes, Cardiac/physiology*
Abstract
How the myocardium undergoes geometric, structural, and molecular alterations that result in an end phenotype as might be seen in patients with dilated cardiomyopathy or after myocardial infarction is still poorly understood. Structural modification of the left ventricle, which occurs during these pathological states, results from long-term changes in loading conditions and is commonly referred to as "remodeling." Remodeling may occur from increased wall stress in the face of hypertensive heart disease, valvular disease, or, perhaps most dramatically, after permanent coronary occlusion. A fundamental derangement of myocyte function is the most common perception for the basis of remodeling, but the role of cells in the heart other than the muscle cell must, of course, be considered. Although studies of the myocyte have been extensive, cardiac fibroblasts have been studied less than myocytes. The fibroblast has a broad range of functions in the myocardium ranging from elaboration and remodeling of the extracellular matrix to communication of a range of signals within the heart, including electrical, chemical, and mechanical ones. Integrins are cell surface receptors that are instrumental in mediating cell-matrix interactions in all cells of the organism, including all types within the myocardium. This review will focus on the role of integrins and related proteins in the remodeling process, with a particular emphasis on the cardiac fibroblast. We will illustrate this function by drawing on 2 unique mouse models with perturbation of proteins linked to integrin function.
Files in This Item:
T200905011.pdf Download
DOI
10.231/JIM.0b013e3181c5e61f
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kang, Seok Min(강석민) ORCID logo https://orcid.org/0000-0001-9856-9227
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/105670
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