Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Jun 15:14:1191517.
doi: 10.3389/fphar.2023.1191517. eCollection 2023.

Mitochondrial homeostasis: a potential target for delaying renal aging

Ming Yang  1   2 , Chongbin Liu  1   2 , Na Jiang  1   2 , Yan Liu  1   2 , Shilu Luo  1   2 , Chenrui Li  1   2 , Hao Zhao  1   2 , Yachun Han  1   2 , Wei Chen  1   2 , Li Li  1   2 , Li Xiao  1   2 , Lin Sun  1   2
Affiliations
Review

Mitochondrial homeostasis: a potential target for delaying renal aging

Ming Yang et al. Front Pharmacol. .

Abstract

Mitochondria, which are the energy factories of the cell, participate in many life activities, and the kidney is a high metabolic organ that contains abundant mitochondria. Renal aging is a degenerative process associated with the accumulation of harmful processes. Increasing attention has been given to the role of abnormal mitochondrial homeostasis in renal aging. However, the role of mitochondrial homeostasis in renal aging has not been reviewed in detail. Here, we summarize the current biochemical markers associated with aging and review the changes in renal structure and function during aging. Moreover, we also review in detail the role of mitochondrial homeostasis abnormalities, including mitochondrial function, mitophagy and mitochondria-mediated oxidative stress and inflammation, in renal aging. Finally, we describe some of the current antiaging compounds that target mitochondria and note that maintaining mitochondrial homeostasis is a potential strategy against renal aging.

Keywords: inflammation; mitochondria; mitophagy; oxidative stress; renal aging.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Renal aging mediated by abnormal mitochondrial homeostasis. Abnormal mitochondrial function, decreased mitophagy and enhanced mitochondria-mediated inflammation accelerate renal aging, decreasing kidney function and the ability to resist adverse external stimuli.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Akiyama H., Barger S., Barnum S., Bradt B., Bauer J., Cole G. M., et al. (2000). Inflammation and Alzheimer's disease. Neurobiol. AGING 21, 383–421. 10.1016/s0197-4580(00)00124-x - DOI - PMC - PubMed
    1. Andrianova N. V., Jankauskas S. S., Zorova L. D., Pevzner I. B., Popkov V. A., Silachev D. N., et al. (2018). Mechanisms of Age-Dependent loss of dietary restriction protective effects in acute kidney injury. CELLS-BASEL 7, 178. 10.3390/cells7100178 - DOI - PMC - PubMed
    1. Annunziata G., Jimenez-Garcia M., Tejada S., Moranta D., Arnone A., Ciampaglia R., et al. (2020). Grape polyphenols ameliorate muscle decline reducing oxidative stress and oxidative damage in aged rats. NUTRIENTS 12, 1280. 10.3390/nu12051280 - DOI - PMC - PubMed
    1. Ashrafi G., Schwarz T. L. (2013). The pathways of mitophagy for quality control and clearance of mitochondria. Cell. DEATH Differ. 20, 31–42. 10.1038/cdd.2012.81 - DOI - PMC - PubMed
    1. Bae E., Kim J. H., Jung M. H., Jang S. J., Lee T. W., Jung S., et al. (2020). Paricalcitol attenuates Contrast-Induced acute kidney injury by regulating mitophagy and senescence. Oxid. Med. Cell. Longev. 2020, 7627934. 10.1155/2020/7627934 - DOI - PMC - PubMed

Grants and funding

This work was supported by the Natural Science Foundation of Hunan Province (2021JC0003).

LinkOut - more resources

-