Intracellular Calcium Homeostasis and Kidney Disease
- 1 June 2021
- journal article
- review article
- Published by Bentham Science Publishers Ltd. in Current Medicinal Chemistry
- Vol. 28 (18), 3647-3665
- https://doi.org/10.2174/0929867327666201102114257
Abstract
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 suffered 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 disregulating 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 promosing therapeutic stratergies 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 to renal diseases. Here, we will introduce the 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 that in the mitochondria-associated endoplasmic reticulum membranes of these renal cells.Funding Information
- National Natural Science Foundation of Hunan Province (2018JJ3785)
This publication has 126 references indexed in Scilit:
- VDAC1-based peptides: novel pro-apoptotic agents and potential therapeutics for B-cell chronic lymphocytic leukemiaCell Death & Disease, 2013
- IP3R2 levels dictate the apoptotic sensitivity of diffuse large B-cell lymphoma cells to an IP3R-derived peptide targeting the BH4 domain of Bcl-2Cell Death & Disease, 2013
- Selective regulation of IP3-receptor-mediated Ca2+ signaling and apoptosis by the BH4 domain of Bcl-2 versus Bcl-XlCell Death & Differentiation, 2011
- Functional distinctions in cytosolic calcium regulation between cells of the glomerular filtration barrierCell Calcium, 2010
- Imaging Interorganelle Contacts and Local Calcium Dynamics at the ER-Mitochondrial InterfaceMolecular Cell, 2010
- Phosphorylation of Nephrin Triggers Ca2+ Signaling by Recruitment and Activation of Phospholipase C-γ1Online Journal of Public Health Informatics, 2009
- Targeting Bcl-2-IP3 Receptor Interaction to Reverse Bcl-2's Inhibition of Apoptotic Calcium SignalsMolecular Cell, 2008
- Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channelsThe Journal of cell biology, 2006
- Structural and functional features and significance of the physical linkage between ER and mitochondriaThe Journal of cell biology, 2006
- A pharmacologic target of G3139 in melanoma cells may be the mitochondrial VDACProceedings of the National Academy of Sciences of the United States of America, 2006