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The roles of calcium-sensing receptor (CaSR) in heavy metals-induced nephrotoxicity

Artikel i vetenskaplig tidskrift
Författare A. A. Kosiba
Y. Wang
Dongfeng Chen
C. K. C. Wong
J. Gu
H. Shi
Publicerad i Life Sciences
Volym 242
ISSN 0024-3205
Publiceringsår 2020
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Språk en
Länkar dx.doi.org/10.1016/j.lfs.2019.11718...
Ämnesord Apoptosis, Autophagy, Calcium-sensing receptor, Heavy metals, Intracellular Ca2+ signaling, Nephrotoxicity
Ämneskategorier Endokrinologi och diabetes

Sammanfattning

The kidney is a vital organ responsible for regulating water, electrolyte and acid-base balance as well as eliminating toxic substances from the blood in the body. Exposure of humans to heavy metals in their natural and occupational environments, foods, water, and drugs has serious implications on the kidney's health. The accumulation of heavy metals in the kidney has been linked to acute or chronic renal injury, kidney stones or even renal cancer, at the expense of expensive treatment options. Therefore, unearthing novel biomarkers and potential therapeutic agents or targets against kidney injury for efficient treatment are imperative. The calcium-sensing receptor (CaSR), a G-protein-coupled receptor (GPCR) is typically expressed in the parathyroid glands and renal tubules. It modulates parathyroid hormone secretion according to the serum calcium (Ca2+) concentration. In the kidney, it modulates electrolyte and water excretion by regulating the function of diverse tubular segments. Notably, CaSR lowers passive and active Ca2+ reabsorption in distal tubules, which facilitates phosphate reabsorption in proximal tubules and stimulates proton and water excretion in collecting ducts. Moreover, at the cellular level, modulation of the CaSR regulates cytosolic Ca2+ levels, reactive oxygen species (ROS) generation and the mitogen-activated protein kinase (MAPK) signaling cascades as well as autophagy and the suppression of apoptosis, an effect predominantly triggered by heavy metals. In this regard, we present a review on the CaSR at the cellular level and its potential as a therapeutic target for the development of new and efficient drugs against heavy metals-induced nephrotoxicity. © 2019 Elsevier Inc.

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