AccScience Publishing / ITPS / Volume 7 / Issue 2 / DOI: 10.36922/itps.1726
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REVIEW

Mitochondria: The master regulator of aging

Pouya Sarvari1* Pourya Sarvari1
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1 Iran National Elite Foundation (INEF), Tehran, Iran
INNOSC Theranostics and Pharmacological Sciences 2024, 7(2), 1726 https://doi.org/10.36922/itps.1726
Submitted: 31 August 2023 | Accepted: 16 November 2023 | Published: 22 February 2024
© 2024 by the Author(s). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/ )
Abstract

Mitochondria are ATP-producing organelles in eukaryotic organisms that serve as the cell’s power plants. Besides, mitochondria are integral to regulating cellular homeostasis and metabolism as a result of their essential roles in reactive oxygen species (ROS) production, bioenergetics, catabolism and anabolism, heme and iron-sulfur biosynthesis, iron and calcium homeostasis, apoptosis and signal transduction, as well as immunity and inflammation. It is well accepted that mitochondria are evolutionarily derived from endosymbiotic alphaproteobacteria within eukaryotic cells adapted for effective energy transduction. Although most of the mitochondrial DNA (mtDNA) is thought to have been transported to the eukaryotic nucleus during evolution, mitochondria may have preserved protein-coding genes within their own DNA. Accumulating data show that a progressive decline of mitochondria regulates aging. The present review aims to outline the role of mitochondria in various aspects of aging, including unfolded protein response, generation of ROS, and the contribution of somatic mtDNA mutations as well as inflammation in aging. Moreover, we propose mitochondria-targeted nanoparticles and mitochondrial genome editing as novel tools to modify mitochondrial genome aberrations.

Keywords
Aging
Heteroplasmy
Mitochondrial DNA
Mitochondrial genome editing
Mitochondrial quality control
Mitochondria-targeted nanoparticles
Mitochondrial unfolded protein response
Reactive oxygen species
Funding
None.
Conflict of interest
The authors declare they have no competing interests.
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