Evidence map›Paper›PMID 11337380›Full record

ArticleThe American journal of pathology2001

Heat stress contributes to the enhancement of cardiac mitochondrial complex activity.

I A Sammut, J Jayakumar, N Latif, S Rothery, N J Severs, R T Smolenski, T E Bates, M H Yacoub

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 90 citations in OpenAlex.

  1. Review
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  7. Skeletal muscle adaptations to heat therapy.Journal of applied physiology (Bethesda, Md. : 1985) · 2020
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  11. Review
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  17. Aging augments mitochondrial susceptibility to heat stress.American journal of physiology. Regulatory, integrative and comparative physiology · 2009
    Article
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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

8 authors at 2 institutions in 1 country.

I A SammutDepartments of Cardiothoracic Surgery, and Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom.
J Jayakumar
N Latif
S Rothery
N J Severs
R T Smolenski
T E Bates
M H Yacoub
Imperial College London · GBUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperthermic stress is known to protect against myocardial dysfunction after ischemia-reperfusion injury. It is unclear however, what energetic mechanisms are affected by the molecular adaptation to heat stress. We hypothesized that mild hyperthermic stress can increase mitochondrial respiratory enzyme activity, affording protection to mitochondrial energetics during prolonged cardiac preservation for transplantation. Rat hearts were excised after heat-stress or sham treatment and subjected to cold cardioplegic arrest and ischemia followed by reperfusion in an ex vivo perfusion system. Cardiac function, mitochondrial respiratory, and complex activities were assessed before and after ischemia. Heat shock protein (Hsp 32, 60, and 72) expression was increased in heat-stressed hearts. This was associated with increased mitochondrial complex activities in heat-stress versus sham-treated groups for complex I-V. During reperfusion, higher complex activities and respiratory control ratios were observed in heat-stressed versus sham-treated groups. Recovery of ventricular function was improved in heat-stressed hearts. Furthermore, mitochondria in reperfused heat-stressed myocardium exhibited intact membranes with packed, parallel, lamellar cristae, whereas in sham-treated myocardium, mitochondria were severely disrupted. This study provides the first evidence of heat-stress-mediated enhancement of mitochondrial energetic capacity. This is associated with increased tolerance to ischemia-reperfusion injury. Protection by heat stress against myocardial dysfunction may be partially due to enhancement of mitochondrial energetics.

Indexed as

AnimalsChaperonin 60Citrate (si)-SynthaseElectron TransportFeverIn Vitro TechniquesMaleMicroscopy, ElectronMitochondria, HeartMyocardial IschemiaMyocardiumRatsRats, Sprague-DawleyChaperonin 60Citrate (si)-Synthase

Identifiers

PMID11337380
PMCPMC1891963
OpenAlexW1997587953

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.