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Kidney disease is a serious health problem that burdens our healthcare system. It is crucial to find the accurate pathogenesis of various types of kidney disease to provide guidance for precise therapies for patients suffering from these diseases. However, the exact molecular mechanisms underlying these diseases have not been fully understood. Disturbance of calcium homeostasis in renal cells plays a fundamental role in the development of various types of kidney disease, such as primary glomerular disease, diabetic nephropathy, acute kidney injury and polycystic kidney disease, through promoting cell proliferation, stimulating extracellular matrix accumulation, aggravating podocyte injury, disrupting cellular energetics as well as dysregulating cell survival and death dynamics. As a result, preventing the disturbance of calcium homeostasis in specific renal cells (such as tubular cells, podocytes and mesangial cells) is becoming one of the most promising therapeutic strategies in the treatment of kidney disease. The endoplasmic reticulum and mitochondria are two vital organelles in this process. Calcium ions cycle between the endoplasmic reticulum and mitochondria at the conjugation of these two organelles known as the mitochondria-associated endoplasmic reticulum membrane, maintaining calcium homeostasis. The pharmacologic modulation of cellular calcium homeostasis can be viewed as a novel therapeutic method for renal diseases. Here, we will introduce calcium homeostasis under physiological conditions and the disturbance of calcium homeostasis in kidney diseases. We will focus on the calcium homeostasis regulation in renal cells (including tubular cells, podocytes and mesangial cells), especially in the mitochondria- associated endoplasmic reticulum membranes of these renal cells. Copyright© Bentham Science Publishers; For any queries, please email at


Na Song, Ming Yang, Hao Zhang, Shi-Kun Yang. Intracellular Calcium Homeostasis and Kidney Disease. Current medicinal chemistry. 2021;28(18):3647-3665

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PMID: 33138745

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