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

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 therapeutic approach in AKI.