Evidence map›Paper›PMID 33717117›Full record

ArticleFrontiers in immunology2021

Pin1 Promotes NLRP3 Inflammasome Activation by Phosphorylation of p38 MAPK Pathway in Septic Shock.

Ruijie Dong, Zhenyi Xue, Guangyue Fan, Na Zhang, Chengzhi Wang, Guangliang Li, Yurong Da

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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  12. Urban Particulate Matter Triggers Meibomian Gland Dysfunction.Investigative ophthalmology & visual science · 2024
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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

7 authors at 2 institutions in 1 country.

Ruijie DongDepartment of Immunology, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, School of Basic Sciences, Tianjin Medical University, Tianjin, China.
Zhenyi XueDepartment of Immunology, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, School of Basic Sciences, Tianjin Medical University, Tianjin, China.
Guangyue FanDepartment of Immunology, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, School of Basic Sciences, Tianjin Medical University, Tianjin, China.
Na ZhangDepartment of Cardiology, Tianjin Medical University General Hospital, Tianjin, China.
Chengzhi WangDepartment of Immunology, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, School of Basic Sciences, Tianjin Medical University, Tianjin, China.
Guangliang LiDepartment of Immunology, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, School of Basic Sciences, Tianjin Medical University, Tianjin, China.
Yurong DaDepartment of Immunology, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, School of Basic Sciences, Tianjin Medical University, Tianjin, China.
Tianjin Medical University · CNTianjin Medical University General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pin1 is the only known peptidyl-prolyl cis-trans isomerase (PPIase) that can specifically recognize and isomerize the phosphorylated Serine/Threonine-Proline (pSer/Thr-Pro) motif, change the conformation of proteins through protein phosphorylation, thus regulate various cellular processes in the body. Pin1 plays an important role in cancer, Alzheimer's disease, and autoimmune diseases. However, the specific mechanism of Pin1 regulation in LPS-induced septic shock is unclear. Here, we found that lack of Pin1 reduced shock mortality and organ damage in mice, and NLRP3 inflammasome activation also was reduced in this process. We further confirmed that Pin1 can affect the expression of NLRP3, ASC, Caspase1, and this process can be regulated through the p38 MAPK pathway. We analyzed that p38 MAPK signaling pathway was highly expressed in septic shock and showed a positive correlation with Pin1 in the Gene Expression Omnibus database. We found that Pin1 could affect the phosphorylation of p38 MAPK, have no obvious difference in extracellular signal-regulated kinases (ERK) and Jun-amino-terminal kinase (JNK) signaling. We further found that Pin1 and p-p38 MAPK interacted, but not directly. In addition, Pin1 deficiency inhibited the cleavage of gasdermin D (GSDMD) and promoted the death of macrophages with LPS treatment, and reduced secretion of inflammatory cytokines including IL-1β and IL-18. In general, our results suggest that Pin1 regulates the NLRP3 inflammasome activation by p38 MAPK signaling pathway in macrophages. Thus, Pin1 may be a potential target for the treatment of inflammatory diseases such as septic shock.

Indexed as

MAP Kinase Signaling SystemAnimalsBiomarkersBiopsyCytokinesDisease Models, AnimalDisease SusceptibilityGene Expression RegulationInflammasomesInflammation MediatorsLipopolysaccharidesMacrophagesMiceMice, KnockoutModels, BiologicalNIMA-Interacting Peptidylprolyl IsomeraseBiomarkersCytokinesInflammasomesInflammation MediatorsLipopolysaccharidesNIMA-Interacting Peptidylprolyl IsomeraseNLR Family, Pyrin Domain-Containing 3 ProteinPin1 protein, mousemacrophagesNLRP3 inflammasomep38 MAPKPin1septic shock

Identifiers

PMID33717117
PMCPMC7947244
OpenAlexW3129946495

What OpenQuestion holds

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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.