Evidence map›Paper›PMID 24224132›Full record

ReviewAmerican journal of cardiovascular disease2013

Mechanisms of load dependency of myocardial ischemia reperfusion injury.

Mahmood S Mozaffari, Jun Yao Liu, Worku Abebe, Babak Baban

Abstract readReview
In one paragraph

Review in American journal of cardiovascular disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

  1. Cardioprotective Role of Captopril: From Basic to Applied Investigations.International journal of molecular sciences · 2025
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Role of NLRP3 Inflammasome in Myocardial Ischemia-Reperfusion Injury and Ventricular Remodeling.Medical science monitor : international medical journal of experimental and clinical research · 2022
    Review
  7. The interplay between mitochondria and store-operated CaJournal of cellular and molecular medicine · 2021
    Review
  8. Irisin Protects Against Hind Limb Ischemia Reperfusion Injury.Drug design, development and therapy · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Organ crosstalk: the potent roles of inflammation and fibrotic changes in the course of organ interactions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  14. Article
  15. Protective Effects ofOxidative medicine and cellular longevity · 2019
    Article
  16. Review
  17. Article
  18. [Establishment of an ex vivo myocardial ischemia-reperfusion model in tree shrews].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018
    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

4 authors.

Mahmood S MozaffariDepartment of Oral Biology, College of Dental Medicine, Georgia Regents University Augusta, Georgia 30912, USA.
Jun Yao Liu
Worku Abebe
Babak Baban

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary artery disease and associated ischemic heart disease are prevalent disorders worldwide. Further, systemic hypertension is common and markedly increases the risk for heart disease. A common denominator of systemic hypertension of various etiologies is increased myocardial load/mechanical stress. Thus, it is likely that high pressure/mechanical stress attenuates the contribution of cardioprotective but accentuates the contribution of cardiotoxic pathways thereby exacerbating the outcome of an ischemia reperfusion insult to the heart. Critical events which contribute to cardiomyocyte injury in the ischemic-reperfused heart include cellular calcium overload and generation of reactive oxygen/nitrogen species which, in turn, promote the opening of the mitochondrial permeability transition pore, an important event in cell death. Increasing evidence also indicates that the myocardium is capable of mounting a robust inflammatory response which contributes importantly to tissue injury. On the other hand, cardioprotective maneuvers of ischemic preconditioning and postconditioning have led to identification of complex web of signaling pathways (e.g., reperfusion injury salvage kinase) which ultimately converge on the mitochondria to exert cytoprotection. The present review is intended to briefly describe mechanisms of cardiac ischemia reperfusion injury followed by a discussion of our work focused on how pressure/mechanical stress modulates endogenous cardiotoxic and cardioprotective mechanisms to ultimately exacerbate ischemia reperfusion injury.

Indexed as

calcium overloadHeartinflammationischemia-reperfusionoxidative/nitrosative stresspressuresignaling mechanismsstem cells

Identifiers

PMID24224132
PMCPMC3819580

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.