Mitochondrial Aging in the Context of Kidney Function

Mitochondria are responsible for producing the chemical energy store molecules, adenosine triphosphate (ATP), used to power cellular processes. Unfortunately, mitochondria become dysfunctional with age, in complex ways and for complex reasons that are not yet fully understood. Mitochondria evolved from symbiotic bacteria, and still act much like bacteria inside the cell. They carry a remnant circular genome, the mitochondrial DNA, they replicate as needed to keep their numbers up, they can fuse together and pass around component parts, they are recycled when worn or damaged by the quality control mechanisms of mitophagy. Within this dynamic system, age-related changes in gene expression and damage to mitochondrial DNA produces a growing loss of function. That in turn impacts the ability of organs in the body to function and maintain themselves.

Aging is an inevitable life process. The ability of aging organs to resist adverse external stimuli decreases, and thus they are more vulnerable to damage. Mitochondrial homeostasis plays an indispensable role in maintaining kidney function, and when mitochondrial function is disturbed, it will accelerate the aging of renal cells. Here, we reviewed the evidence of renal mitochondrial disorders, including abnormal mitochondrial function, abnormal mitophagy, and abnormal activation of oxidative stress and inflammation in renal aging.

Although targeting mitochondria is a potential strategy to slow kidney aging, many questions remain to be addressed, such as what role mitochondrial DNA (mtDNA) plays in renal aging. Although current studies have shown that inhibiting the release of mtDNA can inhibit the activation of inflammation and the occurrence of aging in other tissues and cells, there has been no research on the role of mtDNA in renal aging. Moreover, identifying specific renal mitophagy activators is also needed. Current studies have been conducted on animal and cell models, and there may be significant differences in the aging process and immune system between species that could limit the applicability of these findings to humans. Therefore, the relationship between aging and mitochondrial abnormalities in kidney tissue needs to be clarified in future studies.

When these questions are thoroughly investigated and answered, targeting mitochondria as a strategy to alleviate kidney aging will be viable. In addition, given the importance of mitochondria in biological activity and aging, targeting mitochondria may be a strategy for delaying aging in organs other than the kidney.


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