Evidence map›Paper›PMID 22653992›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012

Ischemia reperfusion injury, KATP channels, and exercise-induced cardioprotection against apoptosis.

John C Quindry, Lindsey Miller, Graham McGinnis, Brian Kliszczewicz, J Megan Irwin, Michael Landram, Zea Urbiztondo, Gayani Nanayakkara, Rajesh Amin

Open access · greenAbstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
4.2field-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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Cardioprotective Effect ofInternational journal of molecular sciences · 2025
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Exercise: Teaching myocytes new tricks.Journal of applied physiology (Bethesda, Md. : 1985) · 2017
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Mechanisms of exercise-induced cardioprotection.Physiology (Bethesda, Md.) · 2014
    Review
  19. Review
  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

9 authors at 2 institutions in 1 country.

John C QuindryCardioprotection Laboratory, Department of Kinesiology, Auburn University, Auburn, Alabama 36830, USA. jcq0001@auburn.edu
Lindsey Miller
Graham McGinnis
Brian Kliszczewicz
J Megan Irwin
Michael Landram
Zea Urbiztondo
Gayani Nanayakkara
Rajesh Amin
Auburn University · USAppalachian State University · US

Funding

Mitochondrial KATP channels, exercise, and cardioprotectionR15HL087256 · NHLBI · AUBURN UNIVERSITY AT AUBURN · PI QUINDRY, JOHN C · 2007 to 2007
$176k
NHLBI NIH HHS HL087256
6 · The paper itself

Abstract

Exercise is a potent stimulus against cardiac ischemia reperfusion (IR) injury, although the protective mechanisms are not completely understood. The study purpose was to examine whether the mitochondrial or sarcolemmal ATP-sensitive potassium channel (mito K(ATP) or sarc K(ATP), respectively) mediates exercise-induced cardioprotection against post-IR cell death and apoptosis. Eighty-six, 4-mo-old male Sprague Dawley rats were randomly assigned to treadmill exercise (Ex; 30 m/min, 3 days, 60 min, ∼70 maximal oxygen uptake) and sedentary (Sed) treatments. Rats were exposed to regional cardiac ischemia (50 min) and reperfusion (120 min) or Sham (170 min; no ligation) surgeries. Exercise subgroups received placebo (saline), 5-hydroxydecanoate (5HD; 10 mg/kg ip), or HMR1098 (10 mg/kg ip) to inhibit mito K(ATP) or sarc K(ATP) channel. Comprehensive outcome assessments included post-IR ECG arrhythmias, cardiac tissue necrosis, redox perturbations, and autophagy biomarkers. No arrhythmia differences existed between exercised and sedentary hearts following extended-duration IR (P < 0.05). The sarc K(ATP) channel was confirmed essential (P = 0.002) for prevention of antinecrotic tissue death with exercise (percent infarct, Sed = 42%; Ex = 20%; Ex5HD = 16%; ExHMR = 42%), although neither the mito K(ATP) (P = 0.177) nor sarc K(ATP) (P = 0.274) channel provided post-IR protection against apoptosis (terminal deoxynucleotidyl transferase deoxy UTP-mediated nick-end labeling-positive nuclei/mm(2), Sham = 1.8 ± 0.5; Sed = 19.4 ± 6.7; Ex = 7.5 ± 4.6; Ex5HD = 14.0 ± 3.9; ExHMR = 11.1 ± 1.8). Exercise preconditioning also appears to preserve basal autophagy levels, as assessed by Beclin 1 (P ≤ 0.001), microtubule-associated protein-1 light-chain 3B ratios (P = 0.020), and P62 (P ≤ 0.001), in the hours immediately following IR. Further research is needed to better understand these findings and corresponding redox changes in exercised hearts.

Indexed as

AnimalsAnti-Arrhythmia AgentsApoptosisApoptosis Regulatory ProteinsAutophagyBeclin-1Decanoic AcidsElectrocardiographyGlucuronidesHydroxy AcidsKATP ChannelsMaleMicrotubule-Associated ProteinsMitochondria, HeartMyocardial Reperfusion InjuryOxygen Consumption5-hydroxydecanoic acidAnti-Arrhythmia AgentsApoptosis Regulatory ProteinsBeclin-1Becn1 protein, ratDecanoic AcidsGlucuronidesGtf2h1 protein, mouseHMR 1098 glucuronideHydroxy AcidsKATP ChannelsMap1lc3b protein, mouseMicrotubule-Associated ProteinsSulfonamidesTranscription FactorsTranscription Factor TFIIH

Identifiers

PMID22653992
PMCPMC3426170
OpenAlexW2164296239

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.