CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury

Yixin Ma; Lili Huang; Zheng Zhang; Pengfei Yang; Qingsong Chen; Xujia Zeng; Fangyan Tan; Chunxia Wang; Xiongzhong Ruan; Xiaohui Liao

doi:10.1016/j.gendis.2022.12.003

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CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury

Full-length article | 更新时间：2024-02-04

- CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury
- Genes & Diseases Vol. 1, Issue 1, Pages: 449-463(2024)
- 作者机构：
  
  1. Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University,Chongqing,China,400010
  2. Department of Cell Biology and Genetics, Chongqing Medical University,Chongqing,China,400016
  3. Centre for Nephrology, Royal Free and University College Medical School, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, United Kingdom
  4. Centre for Lipid Research, Key Laboratory of Molecular Biology on Infectious Diseases, Ministry of Education, Chongqing Medical University,Chongqing,China,400016
  5. Kuanren Laboratory of Translational Lipidology, Centre for Lipid Research, Second Affiliated Hospital of Chongqing Medical University,Chongqing,China,400010
- 作者简介：
- 基金信息：
- DOI：10.1016/j.gendis.2022.12.003
  CLC：
- Published：2024，
  
  Published Online：1 January 2024，
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Yixin Ma, Lili Huang, Zheng Zhang, et al. CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury. [J]. Genes & Diseases 1(1):449-463(2024)
DOI：

Yixin Ma, Lili Huang, Zheng Zhang, et al. CD36 promotes tubular ferroptosis by regulating the ubiquitination of FSP1 in acute kidney injury. [J]. Genes & Diseases 1(1):449-463(2024) DOI： 10.1016/j.gendis.2022.12.003.

摘要

Abstract

Reactive oxidative species (ROS) production-driven ferroptosis plays a role in acute kidney injury (AKI). However

its exact molecular mechanism is poorly understood. Scavenger receptor CD36 has important roles in oxidizing lipids

lipid accumulation

metabolic syndrome

and insulin resistance in chronic kidney disease

but its roles remain unexplored in AKI. The present study investigated the role and mechanism of CD36 in regulating proximal tubular cell ferroptosis and AKI. The expression of CD36 was found to be significantly up-regulated in AKI renal tissues and correlated with renal function

which might serve as an independent biomarker for AKI patients. Moreover

in adult mice subjected to AKI

deletion of CD36 (CD36

−/−

) induced tubular cell ROS accumulation

ferroptosis activation

and renal injury. Mechanistically

combining LC-MS/MS

co-IP

and ubiquitination analyses revealed that CD36 could specifically bind to ferroptosis suppressor protein 1 (FSP1) and regulate its ubiquitination at sites K16 and K24

leading to FSP1 degradation and progression of ferroptosis in AKI. The present results emphasize a novel mechanism of CD36 in cisplatin-induced AKI. The discovery of the special CD36 roles in promoting ferroptosis and AKI development by regulating the ubiquitination of FSP1 in proximal tubular cells may be potential therapeutic targets for AKI. Moreover

CD36 may play a key role in the progression of AKI. Therefore

targeting CD36 may provide a promising treatment option for AKI.

关键词

Keywords

Acute kidney injuryCD36FerroptosisFSP1Ubiquitin-dependent degradation

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