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心脏在各种应激因素诸如心肌梗死、心力衰竭、内分泌紊乱等情况下出现的心肌重构往往伴随着胚胎基因的重新激活。胚胎基因激活在起始阶段是可逆的,但随着时间延长,这一改变将引起心肌组织的病理改变,并导致不可逆的功能失调。其中肌球蛋白重链(myosin heavy chain,MHC),利钠肽类已被视为心肌肥厚的重要分子标志,且其表达水平能影响心肌功能和预后。一些胚胎发育期的转录因子在胚胎基因的激活和调控中发挥重要作用。深入研究胚胎基因再编程,了解从心肌细胞体积增大、肌节增粗到心脏增大、功能失代偿各个病理阶段中心肌转录因子的表达时相性变化,有利于阐明心肌肥厚的分子机制,为探索基因治疗另辟蹊径。文章就心肌重构中的胚胎基因再表达及其调控进行综述。
Myocardial remodeling of the heart under various stress factors such as myocardial infarction, heart failure, endocrine disorders, etc. is often accompanied by the reactivation of embryonic genes. Embryonic gene activation is reversible in the initial stages, but over time, this change causes pathological changes in myocardial tissue and leads to irreversible dysfunction. Among them, myosin heavy chain (MHC) and natriuretic peptide have been regarded as important molecular markers of cardiac hypertrophy, and their expression levels can affect myocardial function and prognosis. Some embryonic developmental transcription factors play an important role in the activation and regulation of embryonic genes. In-depth study of embryonic gene reprogramming, understanding from myocardial cell volume, sarcopenia to the heart increased, decompensated at different stages of the pathological changes in the expression of myocardial transcription factor, is conducive to clarify the molecular mechanism of cardiac hypertrophy, Another way to explore gene therapy. This review summarizes the re-expression of embryonic genes and their regulation in myocardial remodeling.