Evidence map›Paper›PMID 19760284›Full record

ReviewPflugers Archiv : European journal of physiology2010

The role of mitochondrial uncoupling proteins in lifespan.

Marcelo O Dietrich, Tamas L Horvath

Open access · greenAbstract readReview
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 62 citations in OpenAlex.

  1. Molecular Basis of Cardiomyopathies in Type 2 Diabetes.International journal of molecular sciences · 2024
    Review
  2. Article
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  5. Review
  6. Energy Metabolism in the Inner Retina in Health and Glaucoma.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
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  11. Review
  12. Article
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  14. Review
  15. Article
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  17. Mitochondrial roles and cytoprotection in chronic liver injury.Biochemistry research international · 2012
    Article
  18. Review
  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.

Marcelo O DietrichSection of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
Tamas L Horvath
Yale University · US

Funding

Ghrelin in Hypothalamic Regulation of Energy BalanceR01DK060711 · NIDDK · YALE UNIVERSITY · PI HORVATH, TAMAS L · 2002 to 2010
$2.3M
NIDDK NIH HHS R01 DK060711
6 · The paper itself

Abstract

The increased longevity in modern societies raised the attention to biological interventions that could promote a healthy aging. Mitochondria are main organelles involved in the production of adenosine triphosphate (ATP), the energetic substrate for cellular biochemical reactions. The production of ATP occurs through the oxidative phosphorylation of intermediate substrates derived from the breakdown of lipids, sugars, and proteins. This process is coupled to production of oxygen reactive species (ROS) that in excess will have a deleterious role in cellular function. The damage promoted by ROS has been emphasized as one of the main processes involved in senescence. In the last decades, the discovery of specialized proteins in the mitochondrial inner membrane that promote the uncoupling of proton flux (named uncoupling proteins-UCPs) from the ATP synthase shed light on possible mechanisms implicated in the buffering of ROS and consequently in the process of aging. UCPs are responsible for a physiological uncoupling that leads to decrease in ROS production inside the mitochondria. Thus, induction of uncoupling through UCPs could decrease the cellular damage that occurs during aging due to excess of ROS. This review will focus on the evidence supporting these mechanisms.

Indexed as

Adenosine TriphosphateAgingAnimalsElectron TransportEnergy MetabolismHumansIon ChannelsLongevityMitochondriaMitochondrial ProteinsMitochondrial Proton-Translocating ATPasesOxidative PhosphorylationReactive Oxygen SpeciesSuperoxidesUncoupling Protein 1Adenosine TriphosphateIon ChannelsMitochondrial ProteinsMitochondrial Proton-Translocating ATPasesReactive Oxygen SpeciesSuperoxidesUncoupling Protein 1

Identifiers

PMID19760284
PMCPMC2809791
OpenAlexW2009596952

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.