Model showing the role of SNX10 as a modulator of endocytic transport and piecemeal mitophagy. In vitro: Under normal conditions (control), SNX10 localizes to early endosomes (RAB5 and EEA1 positive) and late endosomes (CD63 positive) together with endocytic cargo (as EGFR). SNX10-positive structures are also observed near mitochondria. Upon hypoxia-mimicking conditions (induced by DFP or DMOG) SNX10 vesicles co-localize with CD63, LC3B, and p62 and incorporate selected mitochondrial components (including COX-IV), indicating a role for SNX10 in selective mitochondrial degradation. Upon SNX10 knockdown (SNX10 KD), early endosomes appear smaller and more numerous, with a corresponding reduced degradation of EGFR. In contrast, the turnover of mitochondrial COX-IV and ATP synthase is increased, along with reduced oxygen consumption rate and ATP production, reflecting impaired mitochondrial function. The arrow thicknesses indicate the extent of the different pathways under different conditions. In vivo: In zebrafish larvae, Snx10ab DKO leads to decreased levels of mitochondrial proteins (Cox-IV and Samm50), increased levels of ROS, and elevated cell death in the brain region, as shown by TUNEL staining. The snx10ab DKO–mediated cell death can be rescued by treatment with the antioxidant NAC, suggesting that Snx10 modulates piecemeal mitophagy to limit oxidative stress and maintain mitochondrial homeostasis. NAC; N-acetyl cysteine.