Evidence map›Paper›PMID 33976226›Full record

ArticleNature communications2021

YAP promotes the activation of NLRP3 inflammasome via blocking K27-linked polyubiquitination of NLRP3.

Dan Wang, Yening Zhang, Xueming Xu, Jianfeng Wu, Yue Peng, Jing Li, Ruiheng Luo, Lingmin Huang, Liping Liu, Songlin Yu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 1% 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

99 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Targeting USP47 reprograms macrophage polarization to ameliorate septic peritonitis and promote cutaneous wound healing.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Observational
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

39 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

13 authors at 2 institutions in 1 country.

Dan Wang *Department of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.
Yening Zhang *Department of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.
Xueming XuDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.
Jianfeng WuState Key Laboratory of Cellular Stress Biology Innovation Center for Cell Signaling Network, School of Life Sciences, Xiamen University, Xiamen, Fujian Province, People's Republic of China.
Yue PengDepartment of Critical Care Medicine, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.ORCID 0000-0002-2560-9862
Jing LiDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.
Ruiheng LuoDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.
Lingmin HuangDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.
Liping LiuDepartment of General Surgery, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.ORCID 0000-0001-7921-8018
Songlin YuDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.
Ningjie ZhangDepartment of Blood Transfusion, The Second Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China.
Ben LuDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China. xybenlu@csu.edu.cn.ORCID 0000-0002-8597-0406
Kai ZhaoDepartment of Hematology and Key Laboratory of Non-resolving Inflammation and Cancer of Hunan Province, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, People's Republic of China. kaizhao@csu.edu.cn.ORCID 0000-0002-3889-2118
Central South University · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription coactivator YAP plays a vital role in Hippo pathway for organ-size control and tissue homeostasis. Recent studies have demonstrated YAP is closely related to immune disorders and inflammatory diseases, but the underlying mechanisms remain less defined. Here, we find that YAP promotes the activation of NLRP3 inflammasome, an intracellular multi-protein complex that orchestrates host immune responses to infections or sterile injuries. YAP deficiency in myeloid cells significantly attenuates LPS-induced systemic inflammation and monosodium urate (MSU) crystals-induced peritonitis. Mechanistically, YAP physically interacts with NLRP3 and maintains the stability of NLRP3 through blocking the association between NLRP3 and the E3 ligase β-TrCP1, the latter increases the proteasomal degradation of NLRP3 via K27-linked ubiquitination at lys380. Together, these findings establish a role of YAP in the activation of NLRP3 inflammasome, and provide potential therapeutic target to treat the NLRP3 inflammasome-related diseases.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsbeta-Transducin Repeat-Containing ProteinsCells, CulturedHEK293 CellsHumansInflammasomesLysineMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNLR Family, Pyrin Domain-Containing 3 ProteinPolyubiquitinRNA InterferenceUbiquitinationAdaptor Proteins, Signal Transducingbeta-Transducin Repeat-Containing ProteinsBtrc protein, mouseInflammasomesLysineNLR Family, Pyrin Domain-Containing 3 ProteinPolyubiquitinUbiquitin-Protein LigasesYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID33976226
PMCPMC8113592
OpenAlexW3162932895

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.