Abstract: Cadmium (Cd) as a toxic heavy metal, and the situation of pollution is becoming more and more serious in China. Cd accumulates in kidney after exposure to human body. In the kidney, Cd mainly accumulates in the renal tubules. Due to the long half-life of Cd in human body, Cd will cause the loss or disorder of renal function, and even increase the incidence of renal cancer. At present,  studies have suggested that Cd causes endoplasmic reticulum stress, calcium homeostasis disruption, and eventually leads to cell apoptosis. Ca2+ homeostasis plays a key role in maintaining the normal physiological function of the cells. Recently, the methods and drugs to restore Cd disrupted Ca2+ homeostasis has been tested. Further studies of the roles and the underlying mechanism of Ca2+ in Cd induced nephrotoxicity are urgently needed. This article reviewed the underlying mechanism of Ca2+ in Cd-induced nephrotoxicity, which might provide a new direction for the study of the mechanism of toxicity and detoxification in Cd.

Key words: cadmium, calcium homeostasis, kidney injury, cell apoptosis

摘要： 镉是一种有毒重金属，在我国污染形势日趋严峻。镉被人体摄入后大部分富集于肾脏。在肾脏中，镉主要累积于肾小管。由于镉在人体中的半衰期长，镉的长期累积会造成肾脏功能缺失或紊乱，甚至增加肾癌的发生几率。镉诱导的肾毒性主要是通过调节肾细胞钙离子转运相关蛋白引发钙离子稳态失衡，最终导致细胞凋亡。近年来，恢复镉诱导的钙离子稳态失衡的方法和药物正在不断探索中。钙离子在镉引起肾毒性中的作用机理的深入研究亟待进行。就钙离子在镉诱导的肾毒性中的作用机理进行了概述,为探讨重金属镉的毒性作用与解毒机制提供了新的方向。

关键词: 镉, 钙稳态, 肾损伤, 细胞凋亡