TY - JOUR
T1 - Ventricular remodeling in heart failure
T2 - The role of myocardial collagen
AU - Janicki, J. S.
AU - Brower, G. L.
AU - Henegar, J. R.
AU - Wang, L.
AU - Hunter, P. J.
AU - Rabinowitz, B.
AU - Kessler-Icekson, G.
AU - Arts, T.
AU - Barry, W.
PY - 1995
Y1 - 1995
N2 - Collagen which is present in the myocardium in relatively small amounts is the most abundant structural protein of the connective tissue network. Its structural organization consists of a complex weave of collagen fibers that surrounds and interconnects myocytes, groups of myocytes, muscle fibers and muscle bundles. The conformation of interstitial fibrillar collagen makes it highly resistant to degradation by all proteinases other than specific collagenases. In hearts with myocardial damage secondary to myocardial infarction, chronic ischemia, inflammation, or cardiomyopathy, a complex sequence of compensatory events occur that eventually result in an adverse left ventricular remodeling. This continual state of remodeling is characterized by persistent collagenase activity, fibrillar collagen degradation, and progressive myocyte loss. The net effect is a shift in the balance between collagen synthesis and degradation which leads to an inadequate fibrillar collagen matrix, progressive ventricular dilatation and sphericalization with wall thinning and eventual congestive heart failure.
AB - Collagen which is present in the myocardium in relatively small amounts is the most abundant structural protein of the connective tissue network. Its structural organization consists of a complex weave of collagen fibers that surrounds and interconnects myocytes, groups of myocytes, muscle fibers and muscle bundles. The conformation of interstitial fibrillar collagen makes it highly resistant to degradation by all proteinases other than specific collagenases. In hearts with myocardial damage secondary to myocardial infarction, chronic ischemia, inflammation, or cardiomyopathy, a complex sequence of compensatory events occur that eventually result in an adverse left ventricular remodeling. This continual state of remodeling is characterized by persistent collagenase activity, fibrillar collagen degradation, and progressive myocyte loss. The net effect is a shift in the balance between collagen synthesis and degradation which leads to an inadequate fibrillar collagen matrix, progressive ventricular dilatation and sphericalization with wall thinning and eventual congestive heart failure.
UR - http://www.scopus.com/inward/record.url?scp=0029088235&partnerID=8YFLogxK
U2 - 10.1007/978-1-4615-1893-8_24
DO - 10.1007/978-1-4615-1893-8_24
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C2 - 8540401
AN - SCOPUS:0029088235
SN - 0065-2598
VL - 382
SP - 239
EP - 245
JO - Advances in Experimental Medicine and Biology
JF - Advances in Experimental Medicine and Biology
ER -