Evidence map›Paper›PMID 20345409›Full record

ReviewActa physiologica (Oxford, England)2010

Regulation of skeletal muscle mitochondrial function: genes to proteins.

I R Lanza, K Sreekumaran Nair

Open access · greenAbstract readReview
In one paragraph

Review in Acta physiologica (Oxford, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
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  6. Article
  7. Review
  8. METTL16-mBMC biology · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Effects of atmospherically relevant PMFrontiers in public health · 2025
    Review
  13. Review
  14. Article
  15. Article
  16. Chronological Age Does not Influence Ex-vivo Mitochondrial Respiration and Quality Control in Skeletal Muscle.The journals of gerontology. Series A, Biological sciences and medical sciences · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

I R LanzaEndocrinology Research Unit, Division of Endocrinology, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.
K Sreekumaran Nair
Mayo Clinic in Arizona · US

Funding

MULTIDISCRIPLINARY TRAINING IN DIGESTIVE DISEASEST32DK007198 · NIDDK · MAYO CLINIC ROCHESTER · PI Harmeet Malhi · 1986 to 2026
$8.9M
MECHANISM OF MUSCLE WASTING IN AGING MANR01AG009531 · NIA · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NAIR, K SREEKUMARAN · 1993 to 2014
$8.8M
IN VIVO REGULATION OF PROTEIN TURNOVER BY HORMONESR01DK041973 · NIDDK · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NAIR, K SREEKUMARAN · 1989 to 2014
$7.3M
NIA NIH HHS R01 AG009531NIA NIH HHS R01-AG09531NIDDK NIH HHS R01 DK041973NIDDK NIH HHS R01-DK41973NIDDK NIH HHS T32 DK007198NIDDK NIH HHS T32-DK007198
6 · The paper itself

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.

Indexed as

Muscle, SkeletalAdenosine TriphosphateAgingAnimalsCellular SenescenceDNA, MitochondrialExerciseHeat-Shock ProteinsHormonesHumansMitochondrial ProteinsMitochondria, MuscleMuscle ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhysical EnduranceSignal TransductionAdenosine TriphosphateDNA, MitochondrialHeat-Shock ProteinsHormonesMitochondrial ProteinsMuscle ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanTranscription Factors

Identifiers

PMID20345409
PMCPMC3070482
OpenAlexW1850019235

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.