心肌肥大?凋亡?纤维化?——高血压心肌肥厚中心肌重塑机制

Myocardial Hypertrophy? Apoptosis? Fibrosis?——Mechanisms in Myocardial Remodeling Induced by Hypertensive Myocardial Hypertrophy

心肌肥厚不仅是高血压的并发症,而且也是多种心血管疾病中的后期病理改变,故其很可能是独立于血压之外的一种危险因素,其病理改变主要包括心肌细胞肥大、非心肌细胞增生和间质纤维化,各种病因导致心肌重塑的机制至今还无定论。一直以来心肌细胞肥大及细胞外基质(extracellular matrix, ECM)纤维化是基础研究及临床心肌重塑逆转的两大热点,近来又有资料表明细胞凋亡与增殖不平衡也在心肌重塑中发挥作用。本文就心肌肥厚的病理改变及心肌重塑中的三大机制研究现状作一综述。

Myocardial hypertrophy is not only a complication of the high blood pressure, but also the later stage in many kinds of pathology changes of cardiovascular diseases, So it is one kind of dangerous factor independent on blood pressure, The pathological changes in myocardial hypertrophy include mainly myocardial hyperplasia, extral myocardial cell proliferation and fibrosis, The mechanisms involed in various kinds of causes of cardiac diseases still have no final conclusion so far. The myocardial hypertrophy and the fibrosis in ECM have always been two major focuses on the basic research and clinical myocardial remodeling prevention, Recently more and more materials indicate the unbalance of cell. Apoptosis and proliferation also play an important role. So this article will make a review on the myocardial pathological changes and the three major mechanisms which caused myocardial remodeling.