Mitochondria are essential for aerobic energy production in eukaryotic cells, but they produce reactive oxygen species (ROS) as by-products, which can cause mitochondrial DNA mutations and dysfunction. Mitochondrial damage can also result from disease processes. Maintaining a healthy population of mitochondria is crucial for cellular well-being. Autophagy, particularly mitophagy, is the major degradative pathway for mitochondrial turnover. Recent evidence suggests that mitophagy is a selective process, targeting dysfunctional mitochondria. This review discusses the process of mitophagy, the role of the mitochondrial permeability transition (MPT) in mitophagy, and the importance of mitophagy in the turnover of dysfunctional mitochondria. The MPT, a process involving the opening of non-specific high-conductance pores in the mitochondrial inner membrane, can lead to mitochondrial depolarization and activation of the mitochondrial ATPase. The MPT is regulated by various factors, including calcium levels and ROS. Mitophagy can be induced by nutrient deprivation and photodamage, and it plays a crucial role in maintaining mitochondrial function and genetic integrity. Aging affects mitochondria, leading to increased ROS generation and mtDNA mutations. Mitophagy may be important for the elimination of dysfunctional mitochondria and mutated mtDNA. Caloric restriction, which induces autophagy, may contribute to longevity by enhancing the removal of oxidatively damaged mitochondria and their mutated mtDNA. Understanding the regulatory pathways and signals that control mitophagy is essential for insights into aging and disease pathogenesis.Mitochondria are essential for aerobic energy production in eukaryotic cells, but they produce reactive oxygen species (ROS) as by-products, which can cause mitochondrial DNA mutations and dysfunction. Mitochondrial damage can also result from disease processes. Maintaining a healthy population of mitochondria is crucial for cellular well-being. Autophagy, particularly mitophagy, is the major degradative pathway for mitochondrial turnover. Recent evidence suggests that mitophagy is a selective process, targeting dysfunctional mitochondria. This review discusses the process of mitophagy, the role of the mitochondrial permeability transition (MPT) in mitophagy, and the importance of mitophagy in the turnover of dysfunctional mitochondria. The MPT, a process involving the opening of non-specific high-conductance pores in the mitochondrial inner membrane, can lead to mitochondrial depolarization and activation of the mitochondrial ATPase. The MPT is regulated by various factors, including calcium levels and ROS. Mitophagy can be induced by nutrient deprivation and photodamage, and it plays a crucial role in maintaining mitochondrial function and genetic integrity. Aging affects mitochondria, leading to increased ROS generation and mtDNA mutations. Mitophagy may be important for the elimination of dysfunctional mitochondria and mutated mtDNA. Caloric restriction, which induces autophagy, may contribute to longevity by enhancing the removal of oxidatively damaged mitochondria and their mutated mtDNA. Understanding the regulatory pathways and signals that control mitophagy is essential for insights into aging and disease pathogenesis.