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鼠双微基因2(MDM2)是一原癌基因,因mRNA的不同剪切可形成多种不同相对分子质量的变异体,如p57、p64、p85、p90等。在正常细胞中,MDM2和野生型p53有着精细的平衡,其相互调节形成负反馈回路:p53诱导MDM2表达,MDM2与p53结合形成p53-MDM2复合物,使p53泛素化而被蛋白酶降解。MDM2-p53反馈体系与其他信号转导途径一起形成调控网络,参与细胞生长抑制、凋亡、细胞周期调控等各种生物进程。现对MDM2/p53途径在心血管疾病中的研究进展进行综述。
Mouse double microgene 2 (MDM2) is a proto-oncogene, which can form many different molecular weight variants such as p57, p64, p85, p90 and so on due to different cleavage of mRNA. In normal cells, MDM2 and wild-type p53 have a fine balance and they form a negative feedback loop: p53 induces MDM2 expression, and MDM2 binds to p53 to form the p53-MDM2 complex, which causes ubiquitination of p53 and degradation by proteases. The MDM2-p53 feedback system forms regulatory networks along with other signal transduction pathways and is involved in various biological processes such as cell growth arrest, apoptosis, and cell cycle regulation. The progress of MDM2 / p53 pathway in cardiovascular diseases is reviewed.