Evidence map›Paper›PMID 25726180›Full record

ReviewThe journal of physiological sciences : JPS2015

Contribution of apoptosis in myocardial reperfusion injury and loss of cardioprotection in diabetes mellitus.

Reza Badalzadeh, Behnaz Mokhtari, Raana Yavari

Open access · goldAbstract readReview
In one paragraph

Review in The journal of physiological sciences : JPS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 67 citations in OpenAlex.

  1. Trial
  2. Research progress on PANoptosis in diabetic cardiomyopathy.Journal of physiology and biochemistry · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Mn(III) Porphyrin, MnTnBuOE-2-PyPInternational journal of molecular sciences · 2023
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Selective Inhibition of PKCJournal of diabetes research · 2020
    Article
  17. Article
  18. Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Reza BadalzadehCardiovascular Research Center, Tabriz University of Medical Sciences, Tabriz, Iran, badalzadehr@tbzmed.ac.ir.
Behnaz Mokhtari
Raana Yavari
Tabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic heart disease is one of the major causes of death worldwide. Ischemia is a condition in which blood flow of the myocardium declines, leading to cardiomyocyte death. However, reperfusion of ischemic regions decreases the rate of mortality, but it can also cause later complications. In a clinical setting, ischemic heart disease is always coincident with other co-morbidities such as diabetes. The risk of heart disease increases 2-3 times in diabetic patients. Apoptosis is considered to be one of the main pathophysiological mechanisms of myocardial ischemia-reperfusion injury. Diabetes can disrupt the anti-apoptotic intracellular signaling cascades involved in myocardial protection. Therefore, targeting these changes may be an effective cardioprotective approach in the diabetic myocardium against ischemia-reperfusion injury. In this article, we review the interaction of diabetes with the pathophysiology of myocardial ischemia-reperfusion injury, focusing on the contribution of apoptosis in this context, and then discuss the alterations of pro-apoptotic or anti-apoptotic pathways probably responsible for the loss of cardioprotection in diabetes.

Indexed as

ApoptosisDiabetes ComplicationsHumansInsulin ResistanceIschemic PostconditioningIschemic Preconditioning, MyocardialKATP ChannelsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreModels, CardiovascularMyocardial IschemiaMyocardial Reperfusion InjuryOxidative StressSignal TransductionKATP ChannelsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition Pore

Identifiers

PMID25726180
PMCPMC10717803
OpenAlexW2087361537

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.