Regulated cell death in cisplatin-induced AKI: relevance of myo-inositol metabolism

Fei Deng, Xiaoping Zheng, Isha Sharma, Yingbo Dai, Yinhuai Wang, Yashpal S. Kanwar

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish (US)
Pages (from-to)F578-F595
JournalAmerican journal of physiology. Renal physiology
Volume320
Issue number4
DOIs
StatePublished - Apr 1 2021

Keywords

  • acute kidney injury
  • cisplatin
  • myo-inositol
  • regulated cell death

ASJC Scopus subject areas

  • Physiology
  • Urology

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