Mitochondrial fission/fusion dynamics and apoptosis |
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| Authors: | Clare Sheridan Seamus J. Martin |
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| Affiliation: | 1. Division of Clinical Genetics and Metabolic Disorders, Pediatrics Department, Tawam Hospital, Al-Ain, United Arab Emirates;2. Division of Neurology, Pediatrics Department, Tawam Hospital, Al Ain, United Arab Emirates;3. Medical Genetics Division, King Fahad Medical City, Riyadh, Saudi Arabia;4. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA;5. Texas Children''s Hospital, Houston, TX, USA;6. Joint BCM-CUHK Center of Medical Genetics, Prince of Wales Hospital, ShaTin, Hong Kong Special Administrative Region;1. Max Planck Institute for Biology of Ageing, Cologne, Germany;2. Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany;3. Center for Molecular Medicine, University of Cologne, Cologne, Germany |
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| Abstract: | Mitochondria play an important role in the progression of apoptosis through the release of pro-apoptotic factors, such as cytochrome c, from the mitochondrial intermembrane space. During this process, mitochondrial networks are dramatically reorganised from long filamentous interconnected tubules into small punctate spheres. Whether remodelling of mitochondrial networks is necessary for apoptosis-associated cytochrome c release, or merely an accompanying process, has been a subject of debate. Here we discuss evidence for and against the role of mitochondrial fragmentation in the progression of apoptosis and highlight recent advances which indicate that mitochondrial fission is not a critical requirement for apoptosis-associated cytochrome c release. We also discuss an emerging role for Bcl-2 family members as regulators of mitochondrial fission and fusion dynamics, independent of the role of this family in the regulation of apoptosis. |
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