Martínez Rosas Martín
Departamento de Fisiología, Instituto Nacional de Cardiologia "Ignacio Chávez", México, D.F.
Arch Cardiol Mex. 2006 Oct-Dec;76 Suppl 4:S58-66.
The cardiac remodeling is a progressive response of the heart to acute and chronic insults regardless its etiology. This process is characterized by changes in the size, shape and function and is associated with a worse prognosis in patients with heart failure. The acute myocardial infarction is the most common cause of remodeling. In the first minutes after injury in the ischemic zone there is an important augment in the synthesis and release of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) interleukin-6 (IL-6), interleukin-1-beta (IL-1beta) and transforming growth factor 1-beta (TGF-1beta). This acute releasing of cytokines could regulate the survival or apoptosis of myocytes in infarcted zone and, their negative inotropic effects could represent an adaptative response to delimit the injury and to decrease myocardial energy demand. This significant upregulation of proinflammatory cytokines can extend to noninfarcted zone and triggers a second phase of elevated levels of cytokines that promote interstitial fibrosis and collagen deposition in the contralateral noninfarcted myocardium leading to a dysfunctional ventricle. This article will review the recent reports that support the idea of a cardioprotective role for this early inflammatory response and a deleterious role of the delayed response that mediate the fibrosis that is a typical feature of the remodeling process.
心脏重塑是心脏对急性和慢性损伤的一种渐进性反应，无论其病因如何。这一过程的特征是大小、形状和功能发生变化，并与心力衰竭患者的不良预后相关。急性心肌梗死是重塑最常见的原因。在缺血区损伤后的最初几分钟内，促炎细胞因子如肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、白细胞介素-1-β（IL-1β）和转化生长因子1-β（TGF-1β）的合成和释放显著增加。细胞因子的这种急性释放可调节梗死区心肌细胞的存活或凋亡，其负性变力作用可能代表一种适应性反应，以限制损伤并降低心肌能量需求。促炎细胞因子的这种显著上调可扩展至非梗死区，并引发细胞因子水平升高的第二阶段，从而促进对侧非梗死心肌的间质纤维化和胶原沉积，导致心室功能障碍。本文将综述近期的报告，这些报告支持早期炎症反应具有心脏保护作用的观点，以及延迟反应具有有害作用的观点，延迟反应介导纤维化，而纤维化是重塑过程的典型特征。
