Today’s open access research implicates an imbalance of mitochondrial dynamics in the direction of too much mitochondrial fission in the age-related chronic inflammation observed in endothelial cells of the cardiovascular system. Every cell carries a herd of hundreds of mitochondria, the distant descendants of symbiotic bacteria now integrated as cellular components. The primary task of mitochondria is to generate adenosine triphosphate (ATP), a chemical energy store used to power cellular operations, but they are involved in many core cellular processes. Mitochondria are removed when damaged by the quality control mechanism of mitophagy, and replicate by fission in order to make up their numbers. Mitochondria are very dynamic structures: they pass around component parts, fuse together, and split apart constantly.
A balance between mitochondrial fission and fusion is necessary for optimal cellular function. A sizable portion of the age-related decline in mitochondrial function may be due to an imbalance in the direction of excessive fusion, leading to large mitochondria that become worn and damaged but are resistant to recycling via mitophagy. The proximate cause of this issue appears to be changes in gene expression and protein levels, such as NAD+, or MFF and PUM2, but
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