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Cardiac Extracellular Matrix and Postinfarction Reparative Fibrosis (Part 1). P. 54–66
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Section: Medical and biological sciences
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UDC
611-018.2:616.127-005.8-002.17-06:612.67
Authors
Anna N. Putyatina*, Lena B. Kim*
*Research Institute of Experimental and Clinical Medicine (Novosibirsk, Russian Federation)
Abstract
Modern cardiology has made great progress in the diagnosis of myocardial infarction, high-tech
treatment of patients, and development of new groups of drugs for earliest possible recovery of blood
supply to the ischemic myocardium. However, there remains a serious concern about mortality due
to myocardial infarction, especially in older adults. To improve the situation, it is important to study
the mechanisms of age-related changes in the reactivity of cardiac extracellular matrix and in the
metabolism of its components. This can broaden our understanding of the nature and intensity of cardiac
remodelling. The functionality of cells producing extracellular matrix proteins in response to exogenous
and endogenous factors decreases with age. The quantitative and qualitative composition of cardiac
extracellular matrix components also undergoes changes: collagen and fibronectin content increases,
while the content of proteoglycans/glycosaminoglycans and matricellular proteins decreases, which
is caused by the changing balance in the local regulation system (matrix metalloproteinases/tissue
inhibitors of matrix metalloproteinases) and promotes cardiac interstitial fibrosis. Reparative myocardial
fibrosis has been demonstrated to have different intensity depending on age and comorbidities. Modern
clinical methods of functional assessment of cardiac remodelling in infarction only show changes in
heart structural and functional characteristics and provide little information on the mechanisms of
reparative fibrosis. The following phases can be distinguished in reparative fibrosis progression: the
phase of destructive processes in the extracellular matrix, the phase of peak synthesis of extracellular
matrix proteins, and the reduced synthesis phase. It should be noted that age-dependent modification
of reparative fibrosis often causes the complications of myocardial infarction.
Keywords
extracellular matrix, collagens, proteoglycans, fibronectin, reparative fibrosis, ageing, myocardial infarction
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