Cited by 83Mitochondrial Function and PathologyAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

Regulation of skeletal muscle mitochondrial function: genes to proteins

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Lanza, I. R., Sreekumaran Nair, K.·2010·Acta Physiologica

Abstract

The impact of ageing on mitochondrial function and the deterministic role of mitochondria on senescence continue to be topics of vigorous debate. Many studies report that skeletal muscle mitochondrial content and function are reduced with ageing and metabolic diseases associated with insulin resistance. However, an accumulating body of literature suggests that physical inactivity typical of ageing may be a more important determinant of mitochondrial function than chronological age,per se. Reports of age‐related declines in mitochondrial function have spawned a vast body of literature devoted to understanding the underlying mechanisms. These mechanisms include decreased abundance of mtDNA, reduced mRNA levels, as well as decreased synthesis and expression of mitochondrial proteins, ultimately resulting in decreased function of the whole organelle. Effective therapies to prevent, reverse or delay the onset of the aforementioned mitochondrial changes, regardless of their inevitability or precise underlying causes, require an intimate understanding of the processes that regulate mitochondrial biogenesis, which necessitates the coordinated regulation of nuclear and mitochondrial genomes. Herein we review the current thinking on regulation of mitochondrial biogenesis by transcription factors and transcriptional co‐activators and the role of hormones and exercise in initiating this process. We review how exercise may help preserve mitochondrial content and functionality across the lifespan, and how physical inactivity is emerging as a major determinant of many age‐associated changes at the level of the mitochondrion. We also review evidence that some mitochondrial changes with ageing are independent of exercise or physical activity and appear to be inevitable consequences of old age.

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Crossref · 10.1111/j.1748-1716.2010.02124.x

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  • The relationship between BMI and reduced mitochondrial capacity may be due to the interplay between adiposity and the development of insulin resistance and mitochondrial dysfunction.

    “The relationship between BMI and reduced mitochondrial capacity may be due to the interplay between adiposity and the development of insulin resistance and mitochondrial dysfunction (32) or simply to the lack of physical activity and/or other lifestyle factors.”

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  1. Rennie MJ Anabolic resistance: the effects of aging, sexual dimorphism, and immobilization on human muscle protein turnover Appl Physiol Nutr Metab 2009 34 377 381 19448702

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Authors
Lanza, I. R., & Sreekumaran Nair, K.
Affiliations
Mayo Clinic (US)
Venue
Acta Physiologica
Publisher
Wiley
Published
2010-07
Volume
199
Issue
4
Pages
529-547
ISSN
  • 1748-1708 (ISSN-L)
  • 1748-1716
OpenAlex
W1850019235
Cited by
83
References
155
Citations by year
2026: 3 · 2025: 6 · 2024: 1 · 2022: 1 · 2021: 3 · 2020: 4 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 9 · 2015: 8 · 2014: 9 · 2013: 5 · 2012: 14
FWCI
0.74
Type
journal article
Language
en
Open access
Locations
  • Acta Physiologica (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG009531)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK041973, T32DK007198)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
skeletal muscle, mitochondrial function, mitochondrial biogenesis, aging, physical inactivity, physical activity, insulin resistance, mitochondrial DNA, transcription factors, transcriptional coactivator, hormones, mitochondrial content, cellular senescence
MeSH terms
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Adenosine Triphosphate, Aging, Animals, DNA, Mitochondrial, Heat-Shock Proteins, Hormones, Humans, Mitochondria, Muscle, Muscle Proteins, Physical Endurance, Transcription Factors, Signal Transduction, Exercise, Cellular Senescence, Muscle, Skeletal, Mitochondrial Proteins

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