Evidence map›Paper›PMID 22971741›Full record

ArticleApoptosis : an international journal on programmed cell death2012

Necrosis-like death can engage multiple pro-apoptotic Bcl-2 protein family members.

Denise Tischner, Claudia Manzl, Claudia Soratroi, Andreas Villunger, Gerhard Krumschnabel

Abstract read
In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Mitochondrial Mechanisms of Necroptosis in Liver Diseases.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Redox-Mediated Mechanism of Chemoresistance in Cancer Cells.Antioxidants (Basel, Switzerland) · 2019
    Review
  18. 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

5 authors at 1 institution in 1 country.

Denise Tischner *Division of Developmental Immunology, Biocenter, Medical University Innsbruck, 6020 Innsbruck, Austria.
Claudia Manzl *Division of Developmental Immunology, Biocenter, Medical University Innsbruck, 6020 Innsbruck, Austria.
Claudia SoratroiDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, 6020 Innsbruck, Austria.
Andreas VillungerDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, 6020 Innsbruck, Austria.
Gerhard KrumschnabelDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, 6020 Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

Austrian Science Fund FWF Y 212
6 · The paper itself

Abstract

Necroptosis is a physiologically relevant mode of cell death with some well-described initiating events, but largely unknown executioners. Here we investigated necrostatin-1 (Nec-1) sensitive death elicited by different necroptosis stimuli in L929 mouse fibrosarcoma cells, mouse embryonic fibroblasts (MEF) and bone marrow-derived macrophages. We found that TNFα- or zVAD-induced necroptosis occurs independently of the recently implicated executioners Bmf or PARP-2, but can involve the Bcl-2 family proteins Bid and Bak. Furthermore, this type of necroptosis is associated with mitochondrial cytochrome c release and partly sensitive to cyclosporine A inhibition, suggesting a cross talk with the mitochondrial permeability transition pore. Necroptosis triggered by cadmium (Cd) exposure caused fully Nec-1-sensitive and caspase-independent death in L929 cells that was associated with autocrine TNFα-mediated feed-forward signalling. In MEF Cd-exposure elicited a mixed mode of cell death that was to some extent Nec-1-sensitive but also displayed features of apoptosis. It was partly dependent on Bmf and Bax/Bak, proteins typically considered to act pro-apoptotic, but ultimately insensitive to caspase inhibition. Overall, our study indicates that inducers of "extrinsic" and "intrinsic" necroptosis can both trigger TNF-receptor signalling. Further, necroptosis may depend on mitochondrial changes engaging proteins considered critical for MOMP during apoptosis that ultimately contribute to caspase-independent necrotic cell death.

Indexed as

Adaptor Proteins, Signal TransducingAmino Acid Chloromethyl KetonesAnimalsApoptosisAutocrine CommunicationAutophagybcl-2 Homologous Antagonist-Killer ProteinBH3 Interacting Domain Death Agonist ProteinCadmiumCell LineFibroblastsImidazolesIndolesIntracellular MembranesLysosomesMiceAdaptor Proteins, Signal TransducingAmino Acid Chloromethyl Ketonesbcl-2 Homologous Antagonist-Killer Proteinbenzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketoneBH3 Interacting Domain Death Agonist ProteinBmf protein, mouseCadmiumImidazolesIndolesnecrostatin-1Poly(ADP-ribose) PolymerasesProto-Oncogene Proteins c-bcl-2Receptor-Interacting Protein Serine-Threonine KinasesReceptors, Tumor Necrosis FactorRipk1 protein, mouseRipk3 protein, mouseTumor Necrosis Factor-alpha

Identifiers

PMID22971741
PMCPMC4918797
OpenAlexW2067379222

What OpenQuestion holds

Textmetadata
LicenceTDM
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.