This review article explores the intricate relationship between autophagy, mitochondria, and oxidative stress. Autophagy, a process that degrades damaged cellular components, is crucial for maintaining cellular homeostasis and is regulated by redox signaling. Mitochondria, which generate reactive oxygen species (ROS) and reactive nitrogen species (RNS), are key targets of autophagy. The review highlights how ROS/RNS can damage mitochondria, leading to mitochondrial dysfunction and oxidative stress, which in turn can disrupt autophagy. Recent studies have revealed that autophagy, particularly mitophagy (the autophagic degradation of mitochondria), plays a critical role in maintaining mitochondrial function and preventing oxidative stress. The article discusses the molecular mechanisms of autophagy, including the involvement of Atg proteins and lysosomal hydrolases, and how these processes are regulated by ROS/RNS. It also examines the impact of autophagy on mitochondrial function and the accumulation of reactive species, emphasizing the relevance of these processes in degenerative diseases, particularly neurodegenerative disorders. The review underscores the importance of understanding the cross-talk between autophagy, redox signaling, and mitochondrial dysfunction in the context of disease pathogenesis.This review article explores the intricate relationship between autophagy, mitochondria, and oxidative stress. Autophagy, a process that degrades damaged cellular components, is crucial for maintaining cellular homeostasis and is regulated by redox signaling. Mitochondria, which generate reactive oxygen species (ROS) and reactive nitrogen species (RNS), are key targets of autophagy. The review highlights how ROS/RNS can damage mitochondria, leading to mitochondrial dysfunction and oxidative stress, which in turn can disrupt autophagy. Recent studies have revealed that autophagy, particularly mitophagy (the autophagic degradation of mitochondria), plays a critical role in maintaining mitochondrial function and preventing oxidative stress. The article discusses the molecular mechanisms of autophagy, including the involvement of Atg proteins and lysosomal hydrolases, and how these processes are regulated by ROS/RNS. It also examines the impact of autophagy on mitochondrial function and the accumulation of reactive species, emphasizing the relevance of these processes in degenerative diseases, particularly neurodegenerative disorders. The review underscores the importance of understanding the cross-talk between autophagy, redox signaling, and mitochondrial dysfunction in the context of disease pathogenesis.