Evidence map›Paper›PMID 35770730›Full record

ArticleEMBO reports2022

Functional skewing of TRIM21-SIRT5 interplay dictates IL-1β production in DSS-induced colitis.

Pengbo Yao, Taiqi Chen, Peng Jiang, Li Li, Wenjing Du

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

  1. Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The multifaceted role of sirtuins in inflammatory bowel diseases.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

5 authors at 2 institutions in 1 country.

Pengbo Yao *State Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Department of Cell Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.ORCID 0000-0003-2091-7142
Taiqi Chen *School of Life Sciences, Tsinghua University, Beijing, China.
Peng JiangSchool of Life Sciences, Tsinghua University, Beijing, China.
Li LiState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Department of Cell Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Wenjing DuState Key Laboratory of Medical Molecular Biology, Haihe Laboratory of Cell Ecosystem, Department of Cell Biology, Institute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.ORCID 0000-0002-9761-0774
Chinese Academy of Medical Sciences & Peking Union Medical College · CNTsinghua University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage polarization determines the production of pro- or anti-inflammatory cytokines in response to various bacterial and virus infections. Here, we report that pro-inflammatory macrophage polarization induced by lipopolysaccharide (LPS) skews the TRIM21-SIRT5 interplay toward TRIM21 activation and SIRT5 degradation, resulting in an enhancement of interleukin (IL)-1β production in vitro and in vivo. Mechanistically, LPS challenge enhances the interaction between TRIM21 and SIRT5 to promote SIRT5 ubiquitination and degradation, while reducing the binding of SIRT5 to HAUSP, a deubiquitinating enzyme that stabilizes SIRT5. In a feedback loop, SIRT5 degradation sustains the acetylation of TRIM21 at Lys351, thereby increasing its E3 ligase activity in LPS-activated macrophages. Thus, we identify a functional balance between TRIM21 and SIRT5 that is tilted toward SIRT5 suppression in response to LPS stimulation, thereby enhancing IL-1β production during inflammation.

Indexed as

ColitisInterleukin-1betaRibonucleoproteinsSirtuinsAnimalsCytokinesLipopolysaccharidesMacrophagesUbiquitinationCytokinesInterleukin-1betaLipopolysaccharidesRibonucleoproteinsSirtuinscolitisIL-1βSIRT5TRIM21ubiquitination

Identifiers

PMID35770730
PMCPMC9442300
OpenAlexW4283755962

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.