微小RNAs在心力衰竭炎症机制中作用的研究进展

微小RNA是一组高度保守的长度约22个核苷酸非编码RNA,通过靶定相应的互补序列导致信使RNA的沉默,下调或者抑制翻译以调节基因和蛋白的表达。心力衰竭进程中存在慢性炎症激活和microRNA的异常表达,其中TLR4通路和NF-κB通路被广泛研究和认同,炎症因子如IL-1、IL-6、TNF-α参与心力衰竭的炎症激活过程,并且可以通过多种通路导致心肌细胞肥大,纤维化及凋亡,炎症因子激活、炎症通路中间因子及疾病进展形成复杂的病理网络,最终导致心肌功能紊乱和减退;microRNA可通过部分结合mRNA靶定部分在转录水平上抑制蛋白合成,参与心力衰竭炎症通路的整个过程,这一调节机制在心肌肥大、心力衰竭等多种心脏疾病中的作用逐渐被阐明。本文旨在总结微小RNAs在心力衰竭炎症机制中作用的研究进展,寻找微小RNA与心力衰竭中炎症激活过程的联系。

Effect of the MicroRNAs on the Inflammation Mechanism of Cardiac Failure

MiRNAs are a recently discovered class of highly conserved endogenous small non-coding RNAs, -22 nucleotides in length, that regulate gene and protein expression by binding to partially complementary sequences of mRNA, chronic immune activation and aberrant microRNA （miRNA） expression are present in the progress of a failing heart, the TLR4 and NF-KB pathway has been widely discussed and accepted, Inflammatory cytokines such as IL-1, 6, TNF involved in heart failure inflammatory activation process. Through a variety of pathways leading to cardiac hypertrophy, fibrosis and apoptosis, inflammation factor activation, inflammatory pathways intermediate factor and disease progress form a complex network, eventually leading to myocardial dysfi.mction and deficiency , miRNA translationally repress protein synthesis by binding to partially complementary sequences of mRNA, play a role in the entire process of the inflammation pathway in heart failure. This adjustment mechanism is increasingly clear in cardiac hypertrophy, heart failure and other heart disease. This paper aims to summarize microRNAs participated in two kinds of pathological process and discuss the involvement between microRNAs and the inflammatory activation process in heart failure.