Evidence map›Paper›PMID 36658496›Full record

ArticleBMC molecular and cell biology2023

HMGB1 mediates lipopolysaccharide-induced macrophage autophagy and pyroptosis.

Jiawei Shang, Feng Zhao, Yongmei Cao, Feng Ping, Wei Wang, Yingchuan Li

Open access · goldAbstract read
In one paragraph

Article in BMC molecular and cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.5field-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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Involvement of the pyroptosis-HMGB1 axis in systemic diseases.Frontiers in cell and developmental biology · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. How inflammation influences psychiatric disease.World journal of psychiatry · 2024
    Article
  16. Review
  17. 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

6 authors at 4 institutions in 1 country.

Jiawei Shang *Department of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, 200233, People's Republic of China.
Feng Zhao *Department of Critical Care Medicine, Fudan University Huashan Hospital, Shanghai, 200040, China.
Yongmei Cao *Department of Critical Care Medicine, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China.
Feng PingDepartment of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, 200233, People's Republic of China.
Wei WangDepartment of Critical Care Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, 200233, People's Republic of China. drwangwei3037@126.com.
Yingchuan LiDepartment of Critical Care Medicine, School of Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, 200072, China. yingchuan.li@sjtu.edu.cn.
Shanghai Sixth People's Hospital · CNHuashan Hospital · CNShanghai Tenth People's Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy and pyroptosis of macrophages play important protective or detrimental roles in sepsis. However, the underlying mechanisms remain unclear. High mobility group box protein 1 (HMGB1) is associated with both pyroptosis and autophagy. lipopolysaccharide (LPS) is an important pathogenic factor involved in sepsis. Lentivirus-mediated HMGB1 shRNA was used to inhibit the expression of HMGB1. Macrophages were treated with acetylation inhibitor (AA) to suppress the translocation of HMGB1 from the nucleus to the cytosol. Autophagy and pyroptosis-related protein expressions were detected by Western blot. The levels of caspase-1 activity were detected and the rate of pyroptotic cells was detected by flow cytometry. LPS induced autophagy and pyroptosis of macrophages at different stages, and HMGB1 downregulation decreased LPS-induced autophagy and pyroptosis. Treatment with acetylation inhibitor (anacardic acid) significantly suppressed LPS-induced autophagy, an effect that was not reversed by exogenous HMGB1, suggesting that cytoplasmic HMGB1 mediates LPS-induced autophagy of macrophages. Anacardic acid or an anti-HMGB1 antibody inhibited LPS-induced pyroptosis of macrophages. HMGB1 alone induced pyroptosis of macrophages and this effect was inhibited by anti-HMGB1 antibody, suggesting that extracellular HMGB1 induces macrophage pyroptosis and mediates LPS-induced pyroptosis. In summary, HMGB1 plays different roles in mediating LPS-induced autophagy and triggering pyroptosis according to subcellular localization.

Indexed as

HMGB1 ProteinMacrophagesSepsisAnacardic AcidsAnimalsAutophagyLipopolysaccharidesPyroptosisanacardic acidAnacardic AcidsHMGB1 ProteinLipopolysaccharidesAutophagyHMGB1LipopolysaccharideMacrophagesPyroptosisSubcellular localization

Identifiers

PMID36658496
PMCPMC9854035
OpenAlexW4317503843

What Socratic 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 Socratic graph.