Calcium Signaling Mediates Cell Death and Crosstalk with Autophagy in Kidney Disease

The kidney is an important organ for the maintenance of Ca<sup>2+</sup> homeostasis in the body. However, disruption of Ca<sup>2+</sup> homeostasis will cause a series of kidney diseases, such as acute kidney injury (AKI), chronic kidney disease (CKD), renal ischemia/reperfus...

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Autores principales: Bo Ning, Chuanzhi Guo, Anqi Kong, Kongdong Li, Yimin Xie, Haifeng Shi, Jie Gu
Formato: article
Lenguaje:EN
Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/6b5afc0a9b2243318c096ecdb89eee51
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Sumario:The kidney is an important organ for the maintenance of Ca<sup>2+</sup> homeostasis in the body. However, disruption of Ca<sup>2+</sup> homeostasis will cause a series of kidney diseases, such as acute kidney injury (AKI), chronic kidney disease (CKD), renal ischemia/reperfusion (I/R) injury, autosomal dominant polycystic kidney disease (ADPKD), podocytopathy, and diabetic nephropathy. During the progression of kidney disease, Ca<sup>2+</sup> signaling plays key roles in various cell activities such as necrosis, apoptosis, eryptosis and autophagy. Importantly, there are complex Ca<sup>2+</sup> flux networks between the endoplasmic reticulum (ER), mitochondria and lysosomes which regulate intracellular Ca<sup>2+</sup> signaling in renal cells and contribute to kidney disease. In addition, Ca<sup>2+</sup> signaling also links the crosstalk between various cell deaths and autophagy under the stress of heavy metals or high glucose. In this regard, we present a review of Ca<sup>2+</sup> signaling in cell death and crosstalk with autophagy and its potential as a therapeutic target for the development of new and efficient drugs against kidney diseases.