Parkin, an E3 ubiquitin ligase, is recruited selectively to dysfunctional mitochondria with low membrane potential in mammalian cells. Upon recruitment, Parkin mediates the engulfment of these mitochondria by autophagosomes and their subsequent degradation, promoting autophagy of damaged mitochondria. This process is crucial for maintaining mitochondrial function and integrity, as Parkin loss is associated with mitochondrial dysfunction and increased susceptibility to mitochondrial toxins. The study provides evidence that Parkin's role in mitophagy may contribute to the pathogenesis of Parkinson's disease, where loss of Parkin activity allows the accumulation of dysfunctional mitochondria, leading to neuron loss.Parkin, an E3 ubiquitin ligase, is recruited selectively to dysfunctional mitochondria with low membrane potential in mammalian cells. Upon recruitment, Parkin mediates the engulfment of these mitochondria by autophagosomes and their subsequent degradation, promoting autophagy of damaged mitochondria. This process is crucial for maintaining mitochondrial function and integrity, as Parkin loss is associated with mitochondrial dysfunction and increased susceptibility to mitochondrial toxins. The study provides evidence that Parkin's role in mitophagy may contribute to the pathogenesis of Parkinson's disease, where loss of Parkin activity allows the accumulation of dysfunctional mitochondria, leading to neuron loss.