丝裂原活化蛋白激酶和磷酸酯酶-1在心肌病和细胞凋亡中的作用

The Role of MAPKs and MKP-1 in Cardiomyopathy and Apoptosis of Cardiac Myocyte

ERKJ、NK和p38等丝裂原活化蛋白激酶通过生长因子、激动剂或应激反应等介导生长、分化、凋亡以及细胞间相互作用等多种过程。ERKJ、NK和p38是参与心衰病理过程的主要信号元件,MKP-1是丝裂原活化蛋白激酶等的去磷酸化因子,是一种应激蛋白,在应激反应中可以抑制ERKJ、NK和p38的活性,并通过调节ERK、JNK和p38的活性,参与对心衰病理过程的调节。本文以转基因研究结果为主要线索,对丝裂原活化蛋白激酶和磷酸酯酶-1在心衰病理过程中的作用进行了综述。

Mitogen-activated protein kinases, such as ERK, JNK, and p38, regulate the cell growth, differentiation, apoptosis and cell-cell interaction responding to growth factors, agonists and stress stimuli. Mitogen-activated protein kinases play an important role in the process of the cardiomyopathy and heart failure. Mitogen-activated protein kinase phosphatase-1 is a shock protein to dephosphorylate the mitogen-activated protein kinases. It inhibits the activity of mitogen-activated protein kinases, which is activated by stress stimuli and plays role in the process of heart failure. In this review paper, the roles of mitogen-activated protein kinases and mitogen-activated protein kinase phosphatase-1 were summarized from the in vivo research results of transgenic animal models.