Evidence map›Paper›PMID 35986803›Full record

ReviewApoptosis : an international journal on programmed cell death2022

The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury.

Leonid N Maslov, Sergey V Popov, Natalia V Naryzhnaya, Alexandr V Mukhomedzyanov, Boris K Kurbatov, Ivan A Derkachev, Alla A Boshchenko, Igor Khaliulin, N Rajendra Prasad, Nirmal Singh and 3 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.9field-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

27 citing papers in PubMed, 49 citations in OpenAlex.

  1. Lgr6Genes & diseases · 2026
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  8. Recent advances in the role of gasotransmitters in necroptosis.Apoptosis : an international journal on programmed cell death · 2025
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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

13 authors at 7 institutions in 5 countries.

Leonid N MaslovCardiology Research Institute, Tomsk National Research Medical Centre, The Russian Academy of Sciences, Tomsk, Russia. maslov@cardio-tomsk.ru.
Sergey V PopovCardiology Research Institute, Tomsk National Research Medical Centre, The Russian Academy of Sciences, Tomsk, Russia.
Natalia V NaryzhnayaCardiology Research Institute, Tomsk National Research Medical Centre, The Russian Academy of Sciences, Tomsk, Russia.
Alexandr V MukhomedzyanovCardiology Research Institute, Tomsk National Research Medical Centre, The Russian Academy of Sciences, Tomsk, Russia.
Boris K KurbatovCardiology Research Institute, Tomsk National Research Medical Centre, The Russian Academy of Sciences, Tomsk, Russia.
Ivan A DerkachevCardiology Research Institute, Tomsk National Research Medical Centre, The Russian Academy of Sciences, Tomsk, Russia.
Alla A BoshchenkoCardiology Research Institute, Tomsk National Research Medical Centre, The Russian Academy of Sciences, Tomsk, Russia.
Igor KhaliulinInstitute for Drug Research, School of Pharmacy, Faculty of Medicine, Hebrew University of Jerusalem, Pharmacy Building, Ein Karem, 91120, Jerusalem, Israel.
N Rajendra PrasadDepartment of Biochemistry and Biotechnology, Annamalai University, Annamalainagar, Tamil Nadu, India.
Nirmal SinghDepartment of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India.
Alexei DegterevDepartment of Developmental, Molecular and Chemical Biology, Tufts University School of Medicine, Boston, MA, USA.
Evgenia A TomilovaTyumen State Medical University, Tyumen, Russia.
Ekaterina V SapozhenkovaTyumen State Medical University, Tyumen, Russia.
Tomsk National Research Medical Center · RURussian Academy of Sciences · RUTyumen State Medical University · RUAnnamalai University · INHebrew University of Jerusalem · ILPunjabi University · INTufts University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the last 10 years, mortality from acute myocardial infarction (AMI) has not significantly decreased. This situation is associated with the absence in clinical practice of highly effective drugs capable of preventing the occurrence of reperfusion injury of the heart. Necroptosis inhibitors may become prototypes for the creation of highly effective drugs that increase cardiac tolerance to ischemic/reperfusion (I/R) and reduce the mortality rate in patients with AMI. Necroptosis is involved in I/R cardiac injury and inhibition of RIPK1 or RIPK3 contributes to an increase in cardiac tolerance to I/R. Necroptosis could also be involved in the development of adverse remodeling of the heart. It is unclear whether pre- and postconditioning could inhibit necroptosis of cardiomyocytes and endothelial cells. The role of necroptosis in coronary microvascular obstruction and the no-reflow phenomenon also needs to be studied. MicroRNAs and LncRNAs can regulate necroptotic cell death. Ca

Indexed as

MicroRNAsMyocardial InfarctionRNA, Long NoncodingApoptosisEndothelial CellsHumansNecroptosisProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesReperfusionTOR Serine-Threonine KinasesWaterMicroRNAsProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesRNA, Long NoncodingTOR Serine-Threonine KinasesWaterHeartIschemiaKinasesmicroRNAsNecroptosisReactive oxygen speciesReperfusion

Identifiers

PMID35986803
OpenAlexW4292436426

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.