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介导动脉修复中胶原生物合成和积累的蛋白质:抗再狭窄治疗的新靶点。

Proteins mediating collagen biosynthesis and accumulation in arterial repair: novel targets for anti-restenosis therapy.

机构信息

Schulich Heart Program, Sunnybrook Health Sciences Centre, 2075 Bayview Avenue, Room A-253, Toronto, Ontario, Canada M4N 3M5.

出版信息

Cardiovasc Res. 2011 Jul 1;91(1):16-26. doi: 10.1093/cvr/cvr012. Epub 2011 Jan 18.

DOI:10.1093/cvr/cvr012
PMID:21245059
Abstract

Events contributing to restenosis after coronary interventions include platelet aggregation, inflammatory cell infiltration, growth factor release, and accumulation of smooth muscle cells (SMCs) and extracellular matrix (ECM). The ECM is composed of various collagen subtypes and proteoglycans and over time constitutes the major component of the mature restenotic plaque. The pathophysiology of collagen accumulation in the ECM during arterial restenosis is reviewed. Factors regulating collagen synthesis and degradation, including various cytokines and growth factors involved in the process, may be targets for therapies aimed at prevention of in-stent restenosis.

摘要

动脉再狭窄过程中细胞外基质胶原积累的病理生理学。综述了动脉再狭窄时细胞外基质中胶原积累的病理生理学。调节胶原合成和降解的因素,包括参与该过程的各种细胞因子和生长因子,可能是预防支架内再狭窄治疗的靶点。

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