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生理或病理性刺激会导致心肌肥厚性生长,表现为心肌细胞增大,蛋白合成增加及胎儿基因的再表达。在心脏中有很多信号分子影响着基因表达、细胞凋亡、细胞因子释放等病理生理过程。利用心肌细胞肥厚模型已经发现病理性心肌肥厚可以被抑制或逆转,这些发现为寻找调控心肌肥厚的因子及信号通路提供了基础。该文着重讨论近年来发现的microRNAs(miRNAs)在调节心肌肥厚中的作用。
Physiological or pathological stimuli can lead to hypertrophic cardiac growth, manifested as increased cardiomyocytes, increased protein synthesis and fetal gene re-expression. There are many signaling molecules in the heart that affect the pathophysiology of gene expression, apoptosis, and cytokine release. The use of myocardial cell hypertrophy model has been found that pathological myocardial hypertrophy can be inhibited or reversed, these findings provide a basis for the search for factors and signaling pathways that regulate cardiac hypertrophy. This article focuses on the role of microRNAs (miRNAs) found in recent years in regulating cardiac hypertrophy.