Evidence map›Paper›PMID 26049749›Full record

ReviewCurrent opinion in hematology2015

Fight or flight: regulation of emergency hematopoiesis by pyroptosis and necroptosis.

Ben A Croker, John Silke, Motti Gerlic

Abstract readReview
In one paragraph

Review in Current opinion in hematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. The Zinc Transporter SLC39A10 Plays an Essential Role in Embryonic Hematopoiesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Emerging microbes & infections · 2020
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Alcohol accumulation promotes esophagitis via pyroptosis activation.International journal of biological sciences · 2018
    Article
  16. Article
  17. Review
  18. Review
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

3 authors at 3 institutions in 3 countries.

Ben A CrokeraDivision of Hematology/Oncology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA bThe Walter and Eliza Hall Institute of Medical Research cDepartment of Medical Biology, University of Melbourne, Parkville, Victoria, Australia dDepartment of Clinical Microbiology and Immunology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
John Silke
Motti Gerlic
Boston Children's Hospital · USTel Aviv University · ILUniversity of Melbourne · AU

Funding

Defining the roles of RIPK1 and RIPK3 in emergency hematopoiesisR01HL124209 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CROKER, BEN ADAM · 2015 to 2019
$2.2M
NHLBI NIH HHS 1R01HL124209-01A1NHLBI NIH HHS R01 HL124209
6 · The paper itself

Abstract

purpose of reviewA feature of the innate immune response that is conserved across kingdoms is the induction of cell death. In this review, we discuss the direct and indirect effects of increased inflammatory cell death, including pyroptosis - a caspase-1-dependent cell death - and necroptosis - a receptor-interacting protein kinase 3/mixed lineage kinase domain-like protein-dependent, caspase-independent cell death - on emergency hematopoiesis. RECENT

findingsActivation of nonapoptotic cell death pathways during infection can trigger release of cytokines and/or damage-associated molecular patterns such as interleukin (IL)-1α, IL-1β, IL-18, IL-33, high-mobility group protein B1, and mitochondrial DNA to promote emergency hematopoiesis. During systemic infection, pyroptosis and necroptosis can directly kill hematopoietic stem and progenitor cells, which results in impaired hematopoiesis, cytopenia, and immunosuppression. Although originally described as discrete entities, there now appear to be more intimate connections between the nonapoptotic and death receptor signaling pathways. SUMMARY: The choice to undergo pyroptotic and necroptotic cell death constitutes a rapid response system serving to eliminate infected cells, including hematopoietic stem and progenitor cells. This system has the potential to be detrimental to emergency hematopoiesis during severe infection. We discuss the potential of pharmacological intervention for the pyroptosis and necroptosis pathways that may be beneficial during periods of infection and emergency hematopoiesis.

Indexed as

Caspase 1Cell DeathCytokinesDNA, MitochondrialGene Expression RegulationHematopoiesisHMGB1 ProteinHumansImmunity, InnateInflammationProtein KinasesPyroptosisReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionCaspase 1CytokinesDNA, MitochondrialHMGB1 ProteinHMGB1 protein, humanMLKL protein, humanProtein KinasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK3 protein, human

Identifiers

PMID26049749
PMCPMC4459526
OpenAlexW2201346298

What OpenQuestion holds

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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.