Receptor-mediated mitophagy: An emerging therapeutic target in acute kidney injury

被引：0

作者：

Dagar, Neha ^{[1
]}

Kale, Ajinath ^{[1
]}

Steiger, Stefanie ^{[2
]}

Anders, Hans-Joachim ^{[2
]}

Gaikwad, Anil Bhanudas ^{[1
]}

机构：

[1] Birla Inst Technol & Sci Pilani, Dept Pharm, Lab Mol Pharmacol, Pilani Campus, Pilani 333031, Rajasthan, India

[2] Ludwig Maximilian Univ Munich, Univ Hosp, Dept Internal Med 4, Div Nephrol, D-80336 Munich, Germany

来源：

MITOCHONDRION | 2022年 / 66卷

关键词：

Acute kidney injury; Mitochondria; Mitophagy; Receptor -mediated mitophagy; Mitochondrial fusion; fission; Mitophagy inducers;

D O I：

暂无

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Acute kidney injury (AKI) is a global health concern associated with high morbidity and mortality. AKI etiology is linked to mitochondrial dysfunction along with oxidative stress and inflammation. The defective mitochondria are removed via mitophagy for maintaining cellular integrity. The main regulatory mechanisms of mitophagy in response to different stressors are Phosphatase and tensin homolog-induced kinase 1 (PINK1)/Parkin and receptor-mediated. Receptors like B-cell lymphoma 2/adenovirus E1B-interacting protein (BNIP3), BNIP3L, prohibitin2, tacrolimus (FK506)-binding protein8 (FKBP8), autophagy-beclin1-regulator1 (AMBRA1) and SMAD-ubiquitination regulatory factor1 (SMURF1), etc. participate in receptor-mediated mitophagy. In recent studies, receptor-mediated mitophagy showed protective effects in AKI. This review summarizes the evidence related to mitophagy in AKI and outlines the significance of receptor-mediated mitophagy modulation as a possible ther-apeutic approach in AKI.

引用

页码：82 / 91

页数：10

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