Evidence map›Paper›PMID 31044583›Full record

ReviewCroatian medical journal2019

Necroptosis is one of the modalities of cell death accompanying ischemic brain stroke: from pathogenesis to therapeutic possibilities.

Valentina Hribljan, Damir Lisjak, Dražen Juraj Petrović, Dinko Mitrečić

Open access · diamondAbstract readReview
In one paragraph

Review in Croatian medical journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
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  6. Luteolin-7-Molecules (Basel, Switzerland) · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Progranulin released from microglial lysosomes reduces neuronal ferroptosis after cerebral ischemia in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  11. Review
  12. Article
  13. Article
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  18. Review
  19. The Role of RIPK1 and RIPK3 in Cardiovascular Disease.International journal of molecular sciences · 2020
    Review
  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 at 2 institutions in 2 countries.

Valentina HribljanValentina Hribljan, Laboratory for Stem Cells, Department for Neurogenetics, Medical Genetics and Regenerative Neuroscience, Croatian Institute for Brain Research, University of Zagreb School of Medicine, Šalata 12, HR-10000 Zagreb, Croatia, valentina.hribljan@mef.hr.
Damir Lisjak
Dražen Juraj Petrović
Dinko Mitrečić
Cells Therapy (Poland) · PLUniversity of Zagreb · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to very limited therapeutic options, ischemic brain injury is one of the leading causes of death and lifelong disability worldwide, which imposes enormous public health burden. One of the main events occurring with ischemic brain stroke is cell death. Necroptosis is a type of cell death described as a regulated necrosis characterized by cell membrane disruption mediated by phosphorylated mixed lineage kinase like protein (MLKL). It can be triggered by activation of death receptors (eg, FAS, TNFR1), which lead to receptor-interacting serine/threonine-protein kinase 3 (RIPK3) activation by RIPK1 in the absence of active caspase-8. Here, we review articles that have reported that necroptosis significantly contributes to negative events occurring with the ischemic brain stroke, and that its inhibition is protective both in vitro and in vivo. We also review articles describing positive effects obtained by reducing necroptosis, including the reduction of infarct volume and improved functional recovery in animal models. Since necroptosis is characterized by cell content leakage and subsequent inflammation, in addition to reducing cell death, inhibition of necroptosis in ischemic brain stroke also reduces some inflammatory cytokines. By comparing various approaches in inhibition of necroptosis, we analyze the achieved effects from the perspective of controlling necroptosis as a part of future therapeutic interventions in brain ischemia.

Indexed as

Cell DeathAnimalsApoptosisBrainBrain IschemiaEnzyme InhibitorsHumansInflammationNecrosisPhosphorylationProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesReceptors, Tumor Necrosis Factor, Type IStrokeEnzyme InhibitorsMLKL protein, humanProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesReceptors, Tumor Necrosis Factor, Type IRIPK1 protein, humanRIPK3 protein, humanTNFRSF1A protein, human

Identifiers

PMID31044583
PMCPMC6509625
OpenAlexW2945697674

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.