Mitochondrial fission and fusion are essential for maintaining mitochondrial function under metabolic and environmental stress. Fusion allows damaged mitochondria to share components and compensate for defects, while fission is necessary for creating new mitochondria and removing damaged ones, especially under high stress. Disruptions in these processes can lead to developmental issues and neurodegenerative diseases like Parkinson's. Mitochondria, double-membrane organelles, vary in shape among cell types and undergo continuous changes through fission, fusion, and motility. The balance between fission and fusion rates determines mitochondrial morphology. Fusion proteins like Mfn1, Mfn2, and Opa1 mediate mitochondrial fusion, while Drp1 and Dnm1 are involved in fission. Mitochondrial fusion is crucial for embryonic development and cell survival, but not absolutely necessary in all conditions. Fusion allows damaged mitochondria to share components, and mitochondrial fusion can rescue two mitochondria with mutations in different genes through cross-complementation. Mitochondrial morphology is regulated by metabolism, with increased fusion under oxidative stress and starvation. Mitochondrial damage leads to ROS production, which can be mitigated by quality control mechanisms like proteases and chaperones. Autophagy, or mitophagy, removes damaged mitochondria, and is linked to fission and fusion processes. PINK1 and Parkin pathways identify and eliminate damaged mitochondria by ubiquitinating outer membrane proteins and triggering autophagy. These pathways are critical for mitochondrial quality control and preventing neurodegenerative diseases. Mitochondrial fission and fusion also play roles in apoptosis, with fission facilitating Bax-mediated permeabilization of the outer mitochondrial membrane. Understanding these processes is vital for developing treatments for mitochondrial and neurodegenerative diseases.Mitochondrial fission and fusion are essential for maintaining mitochondrial function under metabolic and environmental stress. Fusion allows damaged mitochondria to share components and compensate for defects, while fission is necessary for creating new mitochondria and removing damaged ones, especially under high stress. Disruptions in these processes can lead to developmental issues and neurodegenerative diseases like Parkinson's. Mitochondria, double-membrane organelles, vary in shape among cell types and undergo continuous changes through fission, fusion, and motility. The balance between fission and fusion rates determines mitochondrial morphology. Fusion proteins like Mfn1, Mfn2, and Opa1 mediate mitochondrial fusion, while Drp1 and Dnm1 are involved in fission. Mitochondrial fusion is crucial for embryonic development and cell survival, but not absolutely necessary in all conditions. Fusion allows damaged mitochondria to share components, and mitochondrial fusion can rescue two mitochondria with mutations in different genes through cross-complementation. Mitochondrial morphology is regulated by metabolism, with increased fusion under oxidative stress and starvation. Mitochondrial damage leads to ROS production, which can be mitigated by quality control mechanisms like proteases and chaperones. Autophagy, or mitophagy, removes damaged mitochondria, and is linked to fission and fusion processes. PINK1 and Parkin pathways identify and eliminate damaged mitochondria by ubiquitinating outer membrane proteins and triggering autophagy. These pathways are critical for mitochondrial quality control and preventing neurodegenerative diseases. Mitochondrial fission and fusion also play roles in apoptosis, with fission facilitating Bax-mediated permeabilization of the outer mitochondrial membrane. Understanding these processes is vital for developing treatments for mitochondrial and neurodegenerative diseases.