Evidence map›Paper›PMID 22935551›Full record

ArticleMechanisms of ageing and development

Impaired adaptability of in vivo mitochondrial energetics to acute oxidative insult in aged skeletal muscle.

Michael P Siegel, Tim Wilbur, Mark Mathis, Eric G Shankland, Atlas Trieu, Mary-Ellen Harper, David J Marcinek

Abstract read
In one paragraph

Article 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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 33 citations in OpenAlex.

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  13. Exercise and CKD: Skeletal Muscle Dysfunction and Practical Application of Exercise to Prevent and Treat Physical Impairments in CKD.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2017
    Review
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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

7 authors at 2 institutions in 2 countries.

Michael P SiegelDepartment of Bioengineering, University of Washington, 3720 15th Ave NE, Seattle, WA 98195, USA. msiegel1@uw.edu
Tim Wilbur
Mark Mathis
Eric G Shankland
Atlas Trieu
Mary-Ellen Harper
David J Marcinek
University of Washington · USUniversity of Ottawa · CA

Funding

SPECIFICITY OF OXYGEN DNA DAMAGE AND MUTAGENESISP01AG001751 · NIA · UNIVERSITY OF WASHINGTON · PI RABINOVITCH, PETER S · 1985 to 2021
$29.6M
University of Washington Nathan Shock Center of Excellence in the Basic Biology of AgingP30AG013280 · NIA · UNIVERSITY OF WASHINGTON · PI Su-In Lee · 1995 to 2026
$27.1M
Mitochondrial Dysfunction in Aged MuscleR01AG028455 · NIA · UNIVERSITY OF WASHINGTON · PI MARCINEK, DAVID J. · 2006 to 2010
$2.0M
Translational Center for In Vivo Mitochondrial MedicineRC2AG036606 · NIA · UNIVERSITY OF WASHINGTON · PI CONLEY, KEVIN E, MARCINEK, DAVID J. · 2009 to 2010
$1.5M
NIA NIH HHS AG001751NIA NIH HHS AG028455NIA NIH HHS AG036606NIA NIH HHS P01 AG001751NIA NIH HHS P30 AG013280NIA NIH HHS R01 AG028455NIA NIH HHS RC2 AG036606
6 · The paper itself

Abstract

Periods of elevated reactive oxygen species (ROS) production are a normal part of mitochondrial physiology. However, little is known about age-related changes in the mitochondrial response to elevated ROS in vivo. Significantly, ROS-induced uncoupling of oxidative phosphorylation has received attention as a negative feedback mechanism to reduce mitochondrial superoxide production. Here we use a novel in vivo spectroscopy system to test the hypothesis that ROS-induced uncoupling is diminished in aged mitochondria. This system simultaneously acquires (31)P magnetic resonance and near-infrared optical spectra to non-invasively measure phosphometabolite and O(2) concentrations in mouse skeletal muscle. Using low dose paraquat to elevate intracellular ROS we assess in vivo mitochondrial function in young, middle aged, and old mice. Oxidative phosphorylation was uncoupled to the same degree in response to ROS at each age, but this uncoupling was associated with loss of phosphorylation capacity and total ATP in old mice only. Using mice lacking UCP3 we demonstrate that this in vivo uncoupling is independent of this putative uncoupler of skeletal muscle mitochondria. These data indicate that ROS-induced uncoupling persists throughout life, but that oxidative stress leads to mitochondrial deficits and loss of ATP in aged organisms that may contribute to impaired function and degeneration.

Indexed as

Oxidative PhosphorylationOxidative StressAdenosine TriphosphateAgingAnimalsFemaleIon ChannelsMiceMice, KnockoutMitochondrial ProteinsMitochondria, MuscleMuscle, SkeletalOxygenReactive Oxygen SpeciesRegenerationUncoupling Protein 3Adenosine TriphosphateIon ChannelsMitochondrial ProteinsOxygenReactive Oxygen SpeciesUcp3 protein, mouseUncoupling Protein 3

Identifiers

PMID22935551
PMCPMC3456966
OpenAlexW2032630678

What OpenQuestion holds

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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.