Evidence map›Paper›PMID 19144753›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009

Aging augments mitochondrial susceptibility to heat stress.

Jodie L Haak, Garry R Buettner, Douglas R Spitz, Kevin C Kregel

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

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  11. Aging impairs induction of redox factor-1 after heat stress: a potential mechanism for heat-induced liver injury.International journal of physiology, pathophysiology and pharmacology · 2015
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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

4 authors at 1 institution in 1 country.

Jodie L HaakDept. of Integrative Physiology, The Univ. of Iowa, Iowa City, 52242, USA.
Garry R Buettner
Douglas R Spitz
Kevin C Kregel
University of Iowa · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Douglas Robert Spitz · 2000 to 2026
$70.0M
OXIDATIVE STRESS AND AGING--INTEGRATED MECHANISMSR01AG012350 · NIA · UNIVERSITY OF IOWA · PI KREGEL, KEVIN CRAIG · 1998 to 2006
$2.4M
Metabolic Oxidative Stress in Human Cancer CellsR01CA100045 · NCI · UNIVERSITY OF IOWA · PI SPITZ, DOUGLAS ROBERT · 2004 to 2008
$1.8M
NCI NIH HHS P30 CA-086862NCI NIH HHS R01 CA-100045NIA NIH HHS R01 AG-12350
6 · The paper itself

Abstract

The pathophysiology of aging is accompanied by a decline in tolerance to environmental stress. While mitochondria are primary suspects in the etiology of aging, little is known about their ability to tolerate perturbations to homeostasis in older organisms. To investigate the role of mitochondria in the increased susceptibility to heat stress that accompanies aging, young and old Fischer 344 rats underwent a heat stress protocol known to elicit exaggerated cellular damage with aging. At either 2 or 24 h after heat stress, livers were removed from animals, and hepatic mitochondria were isolated. Electron microscopy revealed extensive morphological damage to mitochondria from young and, to a greater extent, old rats after heat stress. There was also a significant loss of cytochrome c from old, but not young, mitochondria and a persistent increase in 4-hydroxynonenal-modified proteins in old vs. young mitochondria exposed to heat stress. Electron paramagnetic resonance measurements of superoxide indicate greater superoxide production from mitochondria of old compared with young animals and suggest that mitochondrial integrity was altered during heat stress. The mitochondrial stress response, which functions to correct stress-induced damage to mitochondrial proteins, was also blunted in old rats. Delayed and reduced levels of heat shock protein 60 (Hsp60), the main inducible mitochondrial stress protein, were observed in old compared with young mitochondria after heat stress. Additionally, the amount of Hsp10 protein increased in young, but not old, rat liver mitochondria after hyperthermic challenge. Taken together, these data suggest that mitochondria in old animals are more vulnerable to incurring and less able to repair oxidative damage that occurs in response to a physiologically relevant heat stress.

Indexed as

AgingAldehydesAnimalsBlotting, WesternChaperonin 10Cytochromes cElectron Spin Resonance SpectroscopyHeat-Shock ProteinsHeat Stress DisordersHSP70 Heat-Shock ProteinsMaleMicroscopy, ElectronMitochondria, LiverRatsRats, Inbred F344Reactive Oxygen Species4-hydroxy-2-nonenalAldehydesChaperonin 10Cytochromes cHeat-Shock ProteinsHSP70 Heat-Shock ProteinsReactive Oxygen SpeciesSuperoxides

Identifiers

PMID19144753
PMCPMC2665848
OpenAlexW2058100165

What OpenQuestion holds

Textmetadata
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.