Mitochondria are the power plants of the cell, producing adenosine triphosphate (ATP) to power cellular processes. When mitochondrial function declines all cell functions are negatively affected as a consequence. Many age-related conditions clearly involve mitochondrial dysfunction, particularly in the most energy-hungry tissues, the muscles and the brain.
In addition to damage to the fragile mitochondrial DNA, some forms of which cause a small number of cells to become pathologically broken in ways that actively harms surrounding tissues, all mitochondria throughout the body become more worn and dysfunctional with age. Their dynamics change, the organelles becoming larger and more resistant to the quality control process of mitophagy. The deeper roots of this sweeping decline, and all of the gene expression changes that accompany it, are unclear, but many proximate contributing causes have been identified. Loss of NAD+, reduced expression of mitochondrial fission genes, dysfunction in specific portions of the mitophagy machinery, and so forth.
Efficient skeletal muscle bioenergetics hinge on mitochondria, and mitochondrial dysfunction is recognized as a major hallmark of aging. Indeed, protecting mitochondria is a determinant to preserve proteostasis in skeletal muscle. To
Article originally posted at