Tyagi S C
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA.
J Cell Biochem. 1997 Jun 1;65(3):388-94.
Heart failure secondary to ischemic cardiomyopathy is the primary cause of cardiovascular mortality. The promise of the collateral circulation lies in its potential to alter the course of the natural history of coronary heart disease. The collateral circulation of the heart is responsible for supplying blood and oxygen to the myocardium at ischemic risk following severe stenosis and reduced vasoelasticity function of a major coronary artery. In response to flow, stress, and pressure, collateral vessels are restructured and remodeled. Vascular remodeling by its very nature implies synthesis and degradation of extracellular matrix components in the vessel wall. Under normal physiological conditions proteinases that break down the specialized matrix are tightly regulated by antiproteinases. The balance between proteinase and antiproteinase influences is discoordinated during collateral development which leads to adaptive changes in the structure, function, and regulation of extracellular matrix components in the vessel wall. The role of extracellular matrix components in coronary collateral vessel formation in a canine model of chronic coronary artery occlusion has been demonstrated. The role of matrix proteinases and antiproteinases in the collateral vessel play a significant role in the underlying mechanisms of collateral development. This review presents new and significant information regarding the role of extracellular matrix proteinases and antiproteinases in vascular remodeling, function, and collateral development. Such information will have a significant impact on the understanding of the basic biology of the vascular extracellular matrix turnover, remodeling, and function as well as on elucidating potential avenues for pharmacological approaches designed to increase collateral formation and optimize myocardial blood flow in the treatment of ischemic heart disease.
缺血性心肌病继发的心力衰竭是心血管死亡的主要原因。侧支循环的前景在于其有可能改变冠心病自然病程。心脏侧支循环负责在主要冠状动脉严重狭窄和血管弹性功能降低后，为处于缺血风险的心肌提供血液和氧气。作为对血流、应力和压力的反应，侧支血管会进行重构和重塑。血管重塑本质上意味着血管壁细胞外基质成分的合成和降解。在正常生理条件下，分解特殊基质的蛋白酶受到抗蛋白酶的严格调控。在侧支循环发育过程中，蛋白酶和抗蛋白酶之间的平衡失调，这导致血管壁细胞外基质成分的结构、功能和调节发生适应性变化。细胞外基质成分在犬慢性冠状动脉闭塞模型中冠状动脉侧支血管形成中的作用已得到证实。基质蛋白酶和抗蛋白酶在侧支血管中的作用在侧支循环发育的潜在机制中起重要作用。本综述介绍了有关细胞外基质蛋白酶和抗蛋白酶在血管重塑、功能和侧支循环发育中的作用的新的重要信息。这些信息将对理解血管细胞外基质周转、重塑和功能的基本生物学以及阐明旨在增加侧支循环形成和优化心肌血流以治疗缺血性心脏病的药理学方法的潜在途径产生重大影响。
