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Int. J. Mol. Sci. 2017, 18(7), 1540; doi:10.3390/ijms18071540

Thrombospondins: A Role in Cardiovascular Disease

1
Department of Fundamental and Applied Neurobiology, Serbsky Federal Medical Research Center of Psychiatry and Narcology, 119991 Moscow, Russia
2
Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, 125315 Moscow, Russia
3
Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, 109240 Moscow, Russia
4
Institute for Atherosclerosis Research, Skolkovo Innovative Center, Moscow 121609, Russia
*
Author to whom correspondence should be addressed.
Received: 26 June 2017 / Revised: 5 July 2017 / Accepted: 13 July 2017 / Published: 17 July 2017
(This article belongs to the Special Issue Extracellular Matrix in Development and Disease)
View Full-Text   |   Download PDF [664 KB, uploaded 17 July 2017]   |  

Abstract

Thrombospondins (TSPs) represent extracellular matrix (ECM) proteins belonging to the TSP family that comprises five members. All TSPs have a complex multidomain structure that permits the interaction with various partners including other ECM proteins, cytokines, receptors, growth factors, etc. Among TSPs, TSP1, TSP2, and TSP4 are the most studied and functionally tested. TSP1 possesses anti-angiogenic activity and is able to activate transforming growth factor (TGF)-β, a potent profibrotic and anti-inflammatory factor. Both TSP2 and TSP4 are implicated in the control of ECM composition in hypertrophic hearts. TSP1, TSP2, and TSP4 also influence cardiac remodeling by affecting collagen production, activity of matrix metalloproteinases and TGF-β signaling, myofibroblast differentiation, cardiomyocyte apoptosis, and stretch-mediated enhancement of myocardial contraction. The development and evaluation of TSP-deficient animal models provided an option to assess the contribution of TSPs to cardiovascular pathology such as (myocardial infarction) MI, cardiac hypertrophy, heart failure, atherosclerosis, and aortic valve stenosis. Targeting of TSPs has a significant therapeutic value for treatment of cardiovascular disease. The activation of cardiac TSP signaling in stress and pressure overload may be therefore beneficial. View Full-Text
Keywords: thrombospondins; cardiac remodeling; cardiac hypertrophy; heart failure; atherosclerosis; myocardial infarction; cardiac fibrosis thrombospondins; cardiac remodeling; cardiac hypertrophy; heart failure; atherosclerosis; myocardial infarction; cardiac fibrosis
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Chistiakov, D.A.; Melnichenko, A.A.; Myasoedova, V.A.; Grechko, A.V.; Orekhov, A.N. Thrombospondins: A Role in Cardiovascular Disease. Int. J. Mol. Sci. 2017, 18, 1540.

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