Evidence map›Paper›PMID 32983116›Full record

ReviewFrontiers in immunology2020

The Critical Roles and Mechanisms of Immune Cell Death in Sepsis.

Zhenxing Cheng, Simon T Abrams, Julien Toh, Susan Siyu Wang, Zhi Wang, Qian Yu, Weiping Yu, Cheng-Hock Toh, Guozheng Wang

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
–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

71 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. ACT001 alleviates sepsis-induced acute lung injury by downregulating PANoptosis via the JAK2/STAT3 pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Article
  6. Article
  7. mTOR pathway mediates the endoplasmic reticulum stress -apoptosis of CD4+ T cell through inhibiting autophagy flux in sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  8. Cell death in sepsis: unveiling new perspectives on organ dysfunction.Frontiers in cell and developmental biology · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. TGFBI Inhibits the Pyroptosis of Macrophages to Ameliorate Septic Shock.Journal of cellular and molecular medicine · 2025
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

11 more citing papers are in PubMed but not listed here.

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

9 authors.

Zhenxing ChengDepartment of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom.
Simon T AbramsDepartment of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom.
Julien TohWirral University Teaching Hospitals NHS Foundation Trust, Wirral, United Kingdom.
Susan Siyu WangRoyal London Hospital, London, United Kingdom.
Zhi WangMedical School, Southeast University, Nanjing, China.
Qian YuMedical School, Southeast University, Nanjing, China.
Weiping YuMedical School, Southeast University, Nanjing, China.
Cheng-Hock TohDepartment of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom.
Guozheng WangDepartment of Clinical Infection, Microbiology and Immunology, Institute of Infection and Global Health, University of Liverpool, Liverpool, United Kingdom.

Funding

British Heart Foundation PG/14/19/30751British Heart Foundation PG/16/65/32313
6 · The paper itself

Abstract

Sepsis was first described by the ancient Greek physicians over 2000 years ago. The pathophysiology of the disease, however, is still not fully understood and hence the mortality rate is still unacceptably high due to lack of specific therapies. In the last decade, great progress has been made by shifting the focus of research from systemic inflammatory response syndrome (SIRS) to multiple organ dysfunction syndrome (MODS). Sepsis has been re-defined as infection-induced MODS in 2016. How infection leads to MODS is not clear, but what mediates MODS becomes the major topic in understanding the molecular mechanisms and developing specific therapies. Recently, the mechanism of infection-induced extensive immune cell death which releases a large quantity of damage-associated molecular patterns (DAMPs) and their roles in the development of MODS as well as immunosuppression during sepsis have attracted much attention. Growing evidence supports the hypothesis that DAMPs, including high-mobility group box 1 protein (HMGB1), cell-free DNA (cfDNA) and histones as well as neutrophil extracellular traps (NETs), may directly or indirectly contribute significantly to the development of MODS. Here, we provide an overview of the mechanisms and consequences of infection-induced extensive immune cell death during the development of sepsis. We also propose a pivotal pathway from a local infection to eventual sepsis and a potential combined therapeutic strategy for targeting sepsis.

Indexed as

ApoptosisAlarminsAnimalsApoptosis Regulatory ProteinsBlood CoagulationExtracellular TrapsHost-Pathogen InteractionsHumansImmune SystemMultiple Organ FailureSepsisSignal TransductionAlarminsApoptosis Regulatory Proteinsdamage-associated molecular patterns (DAMPs)extensive immune cell deathextracellular histonesimmunosuppressionmultiple organ dysfunction syndrome (MODS)sepsis

Identifiers

PMID32983116
PMCPMC7477075

What OpenQuestion holds

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Registered trials

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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.