中电导钙激活的K+通道(intermediate—conductanceCa^2+-activatedK^+channel,Kca3.1)最先在红细胞上发现。Kca3.1mRNA和蛋白水平在参与心血管疾病发生的许多细胞中上调,如激活的T细胞、B细胞、巨噬细胞和血小板以及丝裂原刺激的血管平滑肌细胞和成纤维细胞,提示其可能在动脉粥样硬化、再狭窄和心脏纤维化等发生中起作用。本文综述Kca3.1的结构和调控特征、生理作用和在心血管疾病中的病理生理作用,并讨论其阻断剂作为未来心血管疾病治疗靶点的前景。
The intermediate-conductance Ca2+-activated K+ channel (Kca 3.1) was first discovered in erythrocytes. The mRNA and protein levels of Kc, 3.1 are upregulated in numerous types of cells contributing to the development of cardiovascular diseases, such as activated T cells, B cells, macrophages and platelets, mitogen-stimulated vascular smooth muscle cells, and fibroblasts, which suggests a possible role for the channel in atherosclerosis, restenosis and cardiac fibrosis. This article reviews the structure, modulation characteristics, physiological and pathophysiological roles of Kc,3.1 in regulating membrane potential and calcium signaling in cells, and discusses Kca3.1 blocker as a potential therapeutic target for cardiovascular diseases.