The Mechanism of Autophagy Deficiency in Heavy Metal-Induced Nephrotoxicity
A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Toxicology".
Deadline for manuscript submissions: closed (24 October 2023) | Viewed by 359
Special Issue Editor
Special Issue Information
Dear Colleagues,
Heavy metals, such as cadmium (Cd), lead (Pb), arsenic (As), etc., are common environmental contaminants with properties known to be toxic for wildlife and humans. Kidney is the common accumulation site and one key target organ of these heavy metals. Emerging evidence reveals that autophagy is involved in heavy metals-induced nephrotoxicity. It is known that basal autophagy in kidney cells is essential for the maintenance of kidney homeostasis, structure, and function. Under heavy metals exposure, autophagy is overactivated or inhibited to play an important role in the process of kidney injury. Dysregulated autophagy contributes to the pathogenesis of acute kidney injury, to incomplete kidney repair after acute kidney injury, and to chronic kidney disease of varied etiologies. In kidney cells, proximal tubular epithelial cells are the most important target cells for heavy metals exposure, such as Pb, Cd, and As. Kidney proximal tubule epithelial cells have relatively low levels of autophagy under physiological conditions. However, genetic deletion of Atg5 or Atg7 in proximal tubules result in progressive kidney damage. Thus, it is necessary to gain insights into the mechanism of autophagy deficiency and the regulation of autophagy in heavy metal-induced nephrotoxicity and to enable the discovery of pathway-specific and kidney-selective therapies for the prevention of heavy metals-induced kidney diseases.
Prof. Dr. Lin Wang
Guest Editor
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Keywords
- toxicology
- autophagy
- kidney
- proximal tubular cells
- heavy metals
- oxidative stress
- protective effect
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