Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions, leading to abnormal cell processes.

Mitochondria are known for their structural plasticity and undergo fission or fusion depending on specific cellular processes. For instance, mitochondrial fission is associated with mitophagy, a regulatory process that specifically removes damaged mitochondria, thus maintaining tissue homeostasis. However, aging can cause loss or mutation in proteins involved in mitochondrial fission. This eventually impairs mitophagy, a condition often correlated with several age-related diseases such as Alzheimer's disease, Parkinson's disease, cardiomyopathies, and cancer.

In another critical function, mitochondria associates with the cytoskeleton to facilitate their own mobility. It is a crucial factor that enables the distribution of mitochondria across cytoplasms in cells with a complex structure such as neurons. However, in aging cells, the cytoskeleton can become unstable, decreasing the mitochondrial movement and leading to abnormal neuronal functions.

Energy production through respiration is the fundamental function of the mitochondria. The mitochondrial respiratory chains generate superoxide radicals as a toxic byproduct. The mitochondrial antioxidant system typically neutralizes these radicals. However, the aging mitochondria have decreased antioxidant capacity and cannot combat the oxidative stress from the superoxide radicals. This results in the accumulation of reactive oxygen species in the cell that eventually cause cell death.