Evidence map›Paper›PMID 38916095›Full record

ArticleAutophagy2024

Extracellular NCOA4 is a mediator of septic death by activating the AGER-NFKB pathway.

Jiao Liu, Yichun Wang, Ling Zeng, Chunhua Yu, Rui Kang, Daniel J Klionsky, Jianxin Jiang, Daolin Tang

Abstract read
In one paragraph

Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–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

16 citing papers in PubMed.

  1. Article
  2. Review
  3. Structural and molecular principles of DAMP biology.Nature structural & molecular biology · 2026
    Review
  4. Review
  5. Nutrients · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. FPR1-dependent Pro-inflammatory Ccl4Respiratory research · 2025
    Article
  13. Article
  14. Article
  15. Review
  16. 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

8 authors.

Jiao LiuDAMP Laboratory, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Yichun WangDAMP Laboratory, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Ling ZengState Key Laboratory of Trauma, Burns and Combined Injury, Research Institute of Surgery, Daping Hospital, Chongqing, China.
Chunhua YuDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA.
Rui KangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0003-2725-1574
Daniel J KlionskyLife Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA.
Jianxin JiangState Key Laboratory of Trauma, Burns and Combined Injury, Research Institute of Surgery, Daping Hospital, Chongqing, China.
Daolin TangDepartment of Surgery, UT Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0002-1903-6180

Funding

ALTERNATIVE VACUOLAR TARGETING MECHANISMS IN YEASTR01GM053396 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KLIONSKY, DANIEL J. · 1995 to 2018
$12.1M
The mechanism and regulation of autophagyR35GM131919 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DANIEL J. KLIONSKY · 2019 to 2026
$6.4M
Targeting HMGB1-mediated Autophagy in Cancer TherapyR01CA160417 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TANG, DAOLIN · 2012 to 2023
$3.0M
Targeting ACOD1 to attenuate innate immune responses to lethal infectionsR01GM127791 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI Daolin Tang · 2018 to 2026
$2.2M
Mechanisms of Ferroptotic Cancer Cell DeathR01CA229275 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TANG, DAOLIN · 2019 to 2024
$1.8M
The Pancreatic Cancer MicroenvironmentR01CA211070 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI KANG, RUI · 2017 to 2023
$1.4M
NCI NIH HHS R01 CA160417NCI NIH HHS R01 CA211070NCI NIH HHS R01 CA229275NIGMS NIH HHS R01 GM053396NIGMS NIH HHS R01 GM127791NIGMS NIH HHS R35 GM131919
6 · The paper itself

Abstract

Sepsis, a life-threatening condition resulting from a dysregulated response to pathogen infection, poses a significant challenge in clinical management. Here, we report a novel role for the autophagy receptor NCOA4 in the pathogenesis of sepsis. Activated macrophages and monocytes secrete NCOA4, which acts as a mediator of septic death in mice. Mechanistically, lipopolysaccharide, a major component of the outer membrane of Gram-negative bacteria, induces NCOA4 secretion through autophagy-dependent lysosomal exocytosis mediated by ATG5 and MCOLN1. Moreover, bacterial infection with

Indexed as

NF-kappa BNuclear Receptor CoactivatorsSepsisAnimalsAutophagyHumansLipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLSignal TransductionLipopolysaccharidesNCOA4 protein, humanNF-kappa BNuclear Receptor CoactivatorsAutophagy receptorinflammationlysosomal exocytosispattern recognition receptorsepsis

Identifiers

PMID38916095
PMCPMC11587848

What OpenQuestion holds

Textmetadata
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.