期刊
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
卷 320, 期 4, 页码 F578-F595出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.00016.2021
关键词
acute kidney injury; cisplatin; myo-inositol; regulated cell death
资金
- National Institute of Diabetes and Digestive and Kidney Diseases Grant [DK60635]
- China Scholar Council [201706370164]
- National Natural Science Foundation of China [81470925]
- Science and Technology program of Guangdong Scientific Committee [2019A1515012116]
Regulated cell death (RCD), which is distinct from accidental cell death, is a well-controlled programmed cell death process with defined pathological mechanisms. The term RCD encompasses various types of cell death, some of which have been implicated in the pathogenesis of acute kidney injury (AKI), such as cisplatin-induced AKI.
Regulated cell death (RCD), distinct from accidental cell death, refers to a process of well-controlled programmed cell death with well-defined pathological mechanisms. In the past few decades, various terms for RCDs were coined, and some of them have been implicated in the pathogenesis of various types of acute kidney injury (AKI). Cisplatin is widely used as a chemotherapeutic drug for a broad spectrum of cancers, but its usage was hampered because of being highly nephrotoxic. Cisplatin-induced AKI is commonly seen clinically, and it also serves as a well-established prototypic model for laboratory investigations relevant to acute nephropathy affecting especially the tubular compartment. Literature reports over a period of three decades have indicated that there are multiple types of RCDs, including apoptosis, necroptosis, pyroptosis, ferroptosis, and mitochondrial permeability transition-mediated necrosis, and some of them are pertinent to the pathogenesis of cisplatin-induced AKI. Interestingly, myo-inositol metabolism, a vital biological process that is largely restricted to the kidney, seems to be relevant to the pathogenesis of certain forms of RCDs. A comprehensive understanding of RCDs in cisplatin-induced AKI and their relevance to myo-inositol homeostasis may yield novel therapeutic targets for the amelioration of cisplatin-related nephropathy.
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