基质金属蛋白酶与左心室重构及心力衰竭

Matrix metalloproteinase in left ventricular remodeling and heart failure.

作者信息

Shastry Suresh, Hayden Melvin R, Lucchesi Pamela A, Tyagi Suresh C

机构信息

Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA.

出版信息

Curr Cardiol Rep. 2003 May;5(3):200-4. doi: 10.1007/s11886-003-0049-5.

DOI:10.1007/s11886-003-0049-5

PMID:12691636

Abstract

Accumulation of oxidized matrix between the endothelium and cardiac muscle, and endocardial endothelial dysfunction, are the hallmarks of congestive heart failure. The induction of oxidative stress, decrease in endothelial cell density, activation of matrix and disintegrin metalloproteinase, collagenolysis, and repression of cardiac inhibitor of metalloproteinase (CIMP) are associated with deposition of oxidized matrix. Studies that employ CIMP as genetic or proteomic therapeutic agent may improve the heart's response to nitric oxide donors. Identification of major players involved in the control of oxidative and proteolytic stresses that ameliorate matrix deposition by integrin shading will help to develop strategies to prevent congestive heart failure.

摘要

内皮与心肌之间氧化基质的积累以及心内膜内皮功能障碍是充血性心力衰竭的标志。氧化应激的诱导、内皮细胞密度的降低、基质金属蛋白酶和去整合素金属蛋白酶的激活、胶原分解以及金属蛋白酶心脏抑制剂（CIMP）的抑制与氧化基质的沉积有关。将CIMP用作基因或蛋白质组治疗剂的研究可能会改善心脏对一氧化氮供体的反应。确定通过整合素遮蔽改善基质沉积的氧化应激和蛋白水解应激控制中的主要参与者，将有助于制定预防充血性心力衰竭的策略。