The article discusses the critical roles of mitochondrial fission and fusion in maintaining functional mitochondria under metabolic and environmental stresses. Fusion helps mitigate stress by allowing the mixing of contents from partially damaged mitochondria, while fission creates new mitochondria and facilitates the removal of damaged ones, contributing to quality control and apoptosis during high levels of cellular stress. Disruptions in these processes can affect normal development and are implicated in neurodegenerative diseases like Parkinson's. The article also explores the proteins involved in mitochondrial fission and fusion, their regulation, and their roles in complementation between damaged mitochondria, morphology control, and the response to stress. Additionally, it delves into the mechanisms of mitochondrial damage repair, the role of autophagy in eliminating damaged mitochondria, and the involvement of PINK1 and Parkin in quality control and mitophagy. The authors highlight the importance of understanding these processes for developing treatments for mitochondrial and neurodegenerative diseases.The article discusses the critical roles of mitochondrial fission and fusion in maintaining functional mitochondria under metabolic and environmental stresses. Fusion helps mitigate stress by allowing the mixing of contents from partially damaged mitochondria, while fission creates new mitochondria and facilitates the removal of damaged ones, contributing to quality control and apoptosis during high levels of cellular stress. Disruptions in these processes can affect normal development and are implicated in neurodegenerative diseases like Parkinson's. The article also explores the proteins involved in mitochondrial fission and fusion, their regulation, and their roles in complementation between damaged mitochondria, morphology control, and the response to stress. Additionally, it delves into the mechanisms of mitochondrial damage repair, the role of autophagy in eliminating damaged mitochondria, and the involvement of PINK1 and Parkin in quality control and mitophagy. The authors highlight the importance of understanding these processes for developing treatments for mitochondrial and neurodegenerative diseases.