Evidence map›Paper›PMID 35869043›Full record

ReviewCell death & disease2022

Regulated necrosis, a proinflammatory cell death, potentially counteracts pathogenic infections.

Guangzhi Zhang, Jinyong Wang, Zhanran Zhao, Ting Xin, Xuezheng Fan, Qingchun Shen, Abdul Raheem, Chae Rhim Lee, Hui Jiang, Jiabo Ding

Open access · goldAbstract readReview
In one paragraph

Review in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
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  4. Article
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  6. Review
  7. Article
  8. Article
  9. Review
  10. Immune Aging as a Failure of Programmed Cell Death Coordination.International journal of molecular sciences · 2026
    Review
  11. Review
  12. Review
  13. mBio · 2025
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. 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

10 authors at 5 institutions in 2 countries.

Guangzhi Zhang *Institute of Animal Sciences of Chinese Academy of Agricultural Sciences, Beijing, 100193, China.ORCID 0000-0003-4968-5322
Jinyong Wang *Shenzhen Bay Laboratory, Institute of Infectious Diseases, Shenzhen, 518000, China.
Zhanran Zhao *Department of Molecular and Cell Biology and Cancer Research Laboratory, University of California, Berkeley, CA, 94720-3200, USA.
Ting XinInstitute of Animal Sciences of Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
Xuezheng FanInstitute of Animal Sciences of Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
Qingchun ShenInstitute of Animal Sciences of Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
Abdul RaheemInstitute of Animal Sciences of Chinese Academy of Agricultural Sciences, Beijing, 100193, China.
Chae Rhim LeeDepartment of Molecular and Cell Biology and Cancer Research Laboratory, University of California, Berkeley, CA, 94720-3200, USA.
Hui JiangInstitute of Animal Sciences of Chinese Academy of Agricultural Sciences, Beijing, 100193, China. 15011216921@163.com.
Jiabo DingInstitute of Animal Sciences of Chinese Academy of Agricultural Sciences, Beijing, 100193, China. dingjiabo@126.com.ORCID 0000-0002-8515-9031
Chinese Academy of Agricultural Sciences · CNHuazhong Agricultural University · CNJinan University · CNUniversity of California, Berkeley · USUniversity of California, Irvine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since the discovery of cell apoptosis, other gene-regulated cell deaths are gradually appreciated, including pyroptosis, ferroptosis, and necroptosis. Necroptosis is, so far, one of the best-characterized regulated necrosis. In response to diverse stimuli (death receptor or toll-like receptor stimulation, pathogenic infection, or other factors), necroptosis is initiated and precisely regulated by the receptor-interacting protein kinase 3 (RIPK3) with the involvement of its partners (RIPK1, TRIF, DAI, or others), ultimately leading to the activation of its downstream substrate, mixed lineage kinase domain-like (MLKL). Necroptosis plays a significant role in the host's defense against pathogenic infections. Although much has been recognized regarding modulatory mechanisms of necroptosis during pathogenic infection, the exact role of necroptosis at different stages of infectious diseases is still being unveiled, e.g., how and when pathogens utilize or evade necroptosis to facilitate their invasion and how hosts manipulate necroptosis to counteract these detrimental effects brought by pathogenic infections and further eliminate the encroaching pathogens. In this review, we summarize and discuss the recent progress in the role of necroptosis during a series of viral, bacterial, and parasitic infections with zoonotic potentials, aiming to provide references and directions for the prevention and control of infectious diseases of both human and animals.

Indexed as

Communicable DiseasesReceptor-Interacting Protein Serine-Threonine KinasesAnimalsApoptosisCell DeathHumansNecroptosisNecrosisReceptor-Interacting Protein Serine-Threonine Kinases

Identifiers

PMID35869043
PMCPMC9307826
OpenAlexW4286721860

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.