Mitochondrial fission and fusion: A dynamic role in aging and potential target for age-related disease

The mitochondria is the major hub to convert energy for cellular processes. Dysregulation of mitochondrial function is one of the classical telomere(definition) attrition, cellular senescence(definition))." style="text-decoration:underline dotted; text-underline-offset:2px; cursor:help;">hallmarks of aging(definition), and mitochondrial interventions have repeatedly been shown to improve outcomes in age-related diseases. Crucial to mitochondrial regulation is the dynamic nature of their network structure. Mitochondria separate and merge using fission and fusion processes in response to changes in energy and stress status. While many mitochondrial processes are already characterized in relation to aging, specific evidence in multicellular organisms causally linking mitochondrial dynamics to the regulation of lifespan is limited. There does exist, however, a large body of evidence connecting mitochondrial dynamics to other aging-related cellular processes and implicates them in a number of human diseases. Here, we discuss the mechanisms of mitochondrial fission and fusion, the current evidence of their role in aging of multicellular organisms, and how these connect to cell cycle regulation, quality control, and transmission of energy status. Finally, we discuss the current evidence implicating these processes in age-related human pathologies, such as neurodegenerative or cardio-metabolic diseases. We suggest that deeper understanding of the regulatory mechanisms within this system and downstream implications could benefit in understanding and intervention of these conditions.