Evidence map›Paper›PMID 40146485›Full record

ReviewApoptosis : an international journal on programmed cell death2025

Necroptosis in myocardial ischaemia-reperfusion injury: current update on mechanisms, therapeutic targets, and translational potential.

Siarhei A Dabravolski, Vladislav A Kalmykov, Anastasia O Maksaeva, Ulyana V Rozhkova, Ksenia O Lapshina, Alexander N Orekhov

Abstract readReview
PubMed Publisher
In one paragraph

Review in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

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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.

Siarhei A DabravolskiDepartment of Biotechnology Engineering, Braude Academic College of Engineering, Snunit 51, P.O. Box 78, 2161002, Karmiel, Israel. sergedobrowolski@gmail.com.
Vladislav A KalmykovInstitute of General Pathology and Pathophysiology, 8 Baltiyskaya Street, Moscow, Russia, 125315.
Anastasia O MaksaevaInstitute of General Pathology and Pathophysiology, 8 Baltiyskaya Street, Moscow, Russia, 125315.
Ulyana V RozhkovaInstitute of General Pathology and Pathophysiology, 8 Baltiyskaya Street, Moscow, Russia, 125315.
Ksenia O LapshinaFaculty of Biology and Biotechnology, National Research University Higher School of Economics, 33, Profsoyuznaya Street, Building 4, Moscow, Russia, 117418.
Alexander N OrekhovFaculty of Biology and Biotechnology, National Research University Higher School of Economics, 33, Profsoyuznaya Street, Building 4, Moscow, Russia, 117418.

Funding

Russian Science Foundation 25-25-00252
6 · The paper itself

Abstract

Necroptosis is a programmed form of cell death that has gained significant attention in the field of cardiovascular research due to its involvement in myocardial infarction (MI) and myocardial ischaemia-reperfusion (I/R) injury. Unlike apoptosis, necroptosis elicits a pro-inflammatory response, contributing to myocardial injury, fibrosis, and adverse remodelling. This review aims to provide an overview of the molecular mechanisms underlying necroptosis, with a particular focus on its role in myocardial I/R injury. Key regulatory proteins such as Receptor-interacting protein kinase 3 (RIPK3) and Mixed lineage kinase domain-like protein (MLKL) are central to the necroptotic process, mediating cell death and inflammation. The review discusses the potential of targeting necroptosis as a therapeutic strategy for managing cardiovascular diseases, particularly post-MI. The RIPK3-CaMKII-mitochondrial permeability transition pore (mPTP) pathway is identified as a critical signalling axis in necroptosis and its inhibition may offer protective benefits in myocardial injury. The review also considers the role of natural and chemical inhibitors and other genes in necroptosis regulation. Overall, targeting necroptosis represents a promising avenue for therapeutic intervention to mitigate cardiac injury, promote recovery, and improve long-term patient outcomes in cardiovascular diseases.

Indexed as

Myocardial Reperfusion InjuryNecroptosisAnimalsApoptosisHumansMitochondrial Permeability Transition PoreReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionMitochondrial Permeability Transition PoreReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, humanCardiac damageIschaemia-reperfusion injuryMyocardial infarctionNecroptosisRIPK3 inhibitorsRIPK3-MLKL pathway

Identifiers

PMID40146485

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.