Dzau V J
Falk Cardiovascular Research Center, Stanford University School of Medicine, California 94305-5246.
Am J Cardiol. 1992 Oct 8;70(10):4C-11C. doi: 10.1016/0002-9149(92)91352-5.
At the cellular and molecular level the transition to heart failure is a complex process that involves structural adaptation, not only of the heart, but of peripheral vasculature and renal tissues as well. Recent studies have suggested that autocrine, paracrine, and circulating biologically active mediators activate events that result in the concerted failure of adaptive mechanisms and the ultimate depression of cardiac myocyte function. Greater understanding of these local mechanisms in the future may lead to drug therapies that can selectively block these mechanisms and prevent the progression from compensation to overt heart failure.
在细胞和分子水平上，向心力衰竭的转变是一个复杂的过程，不仅涉及心脏的结构适应性改变，还涉及外周血管系统和肾脏组织。最近的研究表明，自分泌、旁分泌和循环中的生物活性介质激活了一系列事件，这些事件导致适应性机制协同失效，最终使心肌细胞功能受到抑制。未来对这些局部机制有更深入的了解，可能会带来能够选择性阻断这些机制并防止从代偿状态发展为明显心力衰竭的药物疗法。
