Evidence map›Paper›PMID 21865543›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2011

Hypercholesterolemia increases mitochondrial oxidative stress and enhances the MPT response in the porcine myocardium: beneficial effects of chronic exercise.

Kyle S McCommis, Allison M McGee, M Harold Laughlin, Douglas K Bowles, Christopher P Baines

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In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

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  17. Mitochondria, cholesterol and cancer cell metabolism.Clinical and translational medicine · 2016
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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

5 authors at 1 institution in 1 country.

Kyle S McCommisDepartment of Biomedical Sciences, University of Missouri-Columbia, Columbia, Missouri 65211, USA.
Allison M McGee
M Harold Laughlin
Douglas K Bowles
Christopher P Baines
University of Missouri · US

Funding

Vascular Biology: Exercise Training and Vascular DiseaseP01HL052490 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI LAUGHLIN, M HAROLD · 1995 to 2010
$19.3M
Molecular Identity of the Cardiac Mitochondrial PoreR01HL094404 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI BAINES, CHRISTOPHER P · 2009 to 2018
$3.6M
NHLBI NIH HHS HL052490NHLBI NIH HHS HL094404NHLBI NIH HHS R01 HL094404
6 · The paper itself

Abstract

Hypercholesterolemia has been suggested to have direct negative effects on myocardial function due to increased reactive oxygen species (ROS) generation and increased myocyte death. Mitochondrial permeability transition (MPT) is a significant mediator of cell death, which is enhanced by ROS generation and attenuated by exercise training. The purpose of this study was to investigate the effect of hypercholesterolemia on the MPT response of cardiac mitochondria. We tested the hypothesis that familial hypercholesterolemic (FH) pigs would have an enhanced MPT response and that exercise training could reverse this phenotype. MPT was assessed by mitochondrial swelling in response to 10-100 μM Ca(2+). FH pigs did show an increased MPT response to Ca(2+) that was associated with decreases in the expression of the putative MPT pore components mitochondrial phosphate carrier (PiC) and cyclophilin-D (CypD). FH also caused increased oxidative stress, depicted by increased protein nitrotyrosylation, as well as decreased levels of reduced GSH in cardiac mitochondria. Expression of the mitochondrial antioxidant enzymes manganese superoxide dismutase (MnSOD), thioredoxin-2 (Trx2), and peroxiredoxin-3 (Prx3) was greatly reduced in the FH pigs. In contrast, cytosolic catalase expression and activity were increased. However, chronic exercise training was able to normalize the MPT response in FH pigs, reduce mitochondrial oxidative stress, and return MnSOD, Trx2, Prx3, and catalase expression/activities to normal. We conclude that FH reduces mitochondrial antioxidants, increases mitochondrial oxidative stress, and enhances the MPT response in the porcine myocardium, and that exercise training can reverse these detrimental alterations.

Indexed as

Exercise TherapyOxidative StressAnimalsAntioxidantsCalciumCatalaseCyclophilinsDisease Models, AnimalGenotypeHydroa VacciniformeMaleMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardiumPeptidyl-Prolyl Isomerase FAntioxidantsCalciumCatalaseCyclophilinsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PorePeptidyl-Prolyl Isomerase FPeroxiredoxin IIIPhosphate Transport ProteinsSuperoxide DismutaseThioredoxins

Identifiers

PMID21865543
PMCPMC3213933
OpenAlexW2056661625

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.