Evidence map›Paper›PMID 35052807›Full record

ReviewBiomedicines2022

Interplay of Oxidative Stress and Necrosis-like Cell Death in Cardiac Ischemia/Reperfusion Injury: A Focus on Necroptosis.

Adriana Adameova, Csaba Horvath, Safa Abdul-Ghani, Zoltan V Varga, M Saadeh Suleiman, Naranjan S Dhalla

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2022. 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
4.2field-weighted citation impact, top 5% 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.

  1. Review
  2. Lgr6Genes & diseases · 2026
    Review
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  5. Review
  6. Review
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  11. Article
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  14. World journal of gastroenterology · 2025
    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

6 authors at 6 institutions in 5 countries.

Adriana AdameovaDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University in Bratislava, 83232 Bratislava, Slovakia.ORCID 0000-0002-9803-043X
Csaba HorvathDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University in Bratislava, 83232 Bratislava, Slovakia.
Safa Abdul-GhaniDepartment of Physiology, Faculty of Medicine, Al-Quds University, Abu Dis P.O. Box 89, Palestine.
Zoltan V VargaHCEMM-SU Cardiometabolic Immunology Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, 1089 Budapest, Hungary.ORCID 0000-0002-2758-0784
M Saadeh SuleimanFaculty of Health Sciences, Bristol Heart Institute, The Bristol Medical School, University of Bristol, Bristol BS8 1TH, UK.ORCID 0000-0001-6080-480X
Naranjan S DhallaInstitute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Center, 351 Tache Avenue, Winnipeg, MB R2H 2A6, Canada.
Al-Quds University · PSComenius University Bratislava · SKSemmelweis University · HUSlovak Academy of Sciences · SKSt. Boniface Hospital · CAUniversity of Bristol · GB

Funding

European Union's Horizon 2020 Research and Innovation Programme No 739593National Research, Development and Innovation Office (NKFIH) of Hungary János Bolyai Research Scholarship of the Hungarian Academy of Sciences.Slovak Research and Development Agency APVV-15-0607, APVV-20-0242VEGA VEGA 1/0016/20
6 · The paper itself

Abstract

Extensive research work has been carried out to define the exact significance and contribution of regulated necrosis-like cell death program, such as necroptosis to cardiac ischemic injury. This cell damaging process plays a critical role in the pathomechanisms of myocardial infarction (MI) and post-infarction heart failure (HF). Accordingly, it has been documented that the modulation of key molecules of the canonical signaling pathway of necroptosis, involving receptor-interacting protein kinases (RIP1 and RIP3) as well as mixed lineage kinase domain-like pseudokinase (MLKL), elicit cardioprotective effects. This is evidenced by the reduction of the MI-induced infarct size, alleviation of myocardial dysfunction, and adverse cardiac remodeling. In addition to this molecular signaling of necroptosis, the non-canonical pathway, involving Ca

Indexed as

apoptosisheart failuremyocardial infarctionnecroptosisnitrosative stressoxidative stress

Identifiers

PMID35052807
PMCPMC8773068
OpenAlexW4205229401

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.