Evidence map›Paper›PMID 20363244›Full record

ReviewMechanisms of ageing and development

Mitochondrial uncoupling and lifespan.

Shona A Mookerjee, Ajit S Divakaruni, Martin Jastroch, Martin D Brand

Abstract readReview
In one paragraph

Review in Mechanisms of ageing and development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Mechanisms of Protection Against Oxidative Stress During Hibernation.International journal of molecular sciences · 2026
    Review
  8. Article
  9. Changes in the brain [NADFrontiers in aging neuroscience · 2026
    Review
  10. Article
  11. Article
  12. Mild Mitochondrial Uncoupling for True Ectopic Lipid Disposal.International journal of molecular sciences · 2025
    Review
  13. Evolutionary diversity of muscle OXPHOS efficiencyProceedings. Biological sciences · 2025
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Plasticity of mitochondrial function safeguards phosphorylating respiration during in vitro simulation of rest-phase hypothermia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article

22 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Shona A MookerjeeBuck Institute for Age Research, Novato, CA 94945 USA. smookerj@buckinstitute.org
Ajit S Divakaruni
Martin Jastroch
Martin D Brand
Buck Institute for Research on Aging · US

Funding

PROTEOMICSP01AG025901 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI GIBSON, BRADFORD WAYNE · 2007 to 2011
$8.6M
Mass spectrometry and imaging technologies in GerosciencePL1AG032118 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI GIBSON, BRADFORD WAYNE · 2007 to 2011
$4.5M
Core--RESEARCH DEVELOPMENTP30AG025708 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI CAMPISI, JUDITH · 2005 to 2009
$3.7M
Mitochondrial sites of reactive oxygen species generation in cells.R01AG033542 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI BRAND, MARTIN D · 2009 to 2010
$970k
NIA NIH HHS P01 AG025901NIA NIH HHS P30 AG025708NIA NIH HHS PL1 AG032118NIA NIH HHS R01 AG033542
6 · The paper itself

Abstract

The quest to understand why we age has given rise to numerous lines of investigation that have gradually converged to include metabolic control by mitochondrial activity as a major player. That is, the ideal balance between nutrient uptake, its transduction into usable energy, and the mitigation of damaging byproducts can be regulated by mitochondrial respiration and output (ATP, reactive oxygen species (ROS), and heat). Mitochondrial inefficiency through proton leak, which uncouples substrate oxidation from ADP phosphorylation, can comprise as much as 30% of the basal metabolic rate. This uncoupling is hypothesized to protect cells from conditions that favor ROS production. Uncoupling can also occur through pharmacological induction of proton leak and activity of the uncoupling proteins. Mitochondrial uncoupling is implicated in lifespan extension through its effects on metabolic rate and ROS production. However, evidence to date does not suggest a consistent role for uncoupling in lifespan. The purpose of this review is to discuss recent work examining how mitochondrial uncoupling impacts lifespan.

Indexed as

Energy MetabolismLongevityAdenosine TriphosphateAge FactorsAgingAnimalsCaloric RestrictionGlucoseHumansInsulinMitochondriaMitochondrial ProteinsOxidative StressReactive Oxygen SpeciesAdenosine TriphosphateGlucoseInsulinMitochondrial ProteinsReactive Oxygen Species

Identifiers

PMID20363244
PMCPMC2924931
OpenAlexW2061352989

What OpenQuestion holds

Textmetadata
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.