Evidence map›Paper›PMID 36166295›Full record

ArticleJCI insight2022

Interleukin-37 protects against acinar cell pyroptosis in acute pancreatitis.

Nan Ma, Chenchen Yuan, Juanjuan Shi, Qingtian Zhu, Yang Liu, Xiaojie Ma, Baiqiang Li, Weijuan Gong, Jing Xue, Guotao Lu and 2 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  8. Src Reduces Neutrophil Extracellular Traps Generation and Resolves Acute Organ Damage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

12 authors at 4 institutions in 2 countries.

Nan MaDepartment of Critical Care Medicine, Research Institute of General Surgery, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Chenchen YuanPancreatic Center, Department of Gastroenterology, and.
Juanjuan ShiState Key Laboratory of Oncogenes and Related Genes, Stem Cell Research Centre, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Qingtian ZhuPancreatic Center, Department of Gastroenterology, and.
Yang LiuDepartment of Critical Care Medicine, Jinling Hospital, Medical School of Southeast University, Nanjing, China.
Xiaojie MaDepartment of Critical Care Medicine, Research Institute of General Surgery, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Baiqiang LiDepartment of Critical Care Medicine, Research Institute of General Surgery, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Weijuan GongPancreatic Center, Department of Gastroenterology, and.
Jing XueState Key Laboratory of Oncogenes and Related Genes, Stem Cell Research Centre, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Guotao LuPancreatic Center, Department of Gastroenterology, and.
Weiqin LiDepartment of Critical Care Medicine, Research Institute of General Surgery, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Jieshou LiDepartment of Critical Care Medicine, Research Institute of General Surgery, Affiliated Jinling Hospital, Medical School of Nanjing University, Nanjing, China.
Nanjing Medical University · CNPancreas Centre (Canada) · CAShanghai Jiao Tong University · CNSoutheast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute pancreatitis (AP) is a local and/or systemic inflammatory disease that starts with acinar cell injury and necrosis; it has no effective medical treatment and thus remains a life-threatening condition. Interleukin-37 (IL-37), a natural immunomodulator, has demonstrated an antiinflammatory effect; however, the role of IL-37 in AP remains unknown. The serum IL-37 levels of 39 healthy controls and 94 patients with AP were measured. Cholecystokinin was applied to induce pancreatic acinar cell injury in vitro. Classical experimental AP models, such as caerulein, l-arginine, and taurolithocholic acid 3-sulfate disodium salt, were included in the in vivo study. A transgenic mouse model with the IL-37 gene and administration of recombinant IL-37 were used to further investigate the function of IL-37 in AP. Pancreas-specific gasdermin D-knockout (GSDMD-knockout) mice were used to explore the protective mechanism of IL-37. Our results showed that serum IL-37 levels in humans were negatively correlated with the severity of AP. Furthermore, IL-37-transgenic mice and supplementation with recombinant IL-37 could both protect against AP. Mechanistically, IL-37 was able to suppress pyroptosis of injured acinar cells, and specific depletion of GSDMD in the pancreas counteracted the protective effect of IL-37. Our study demonstrates that IL-37 protects against acinar cell pyroptosis in AP.

Indexed as

Acinar CellsPancreatitisAcute DiseaseAnimalsHumansInterleukin-1InterleukinsMiceMice, KnockoutMice, TransgenicPyroptosisIL37 protein, humanInterleukin-1InterleukinsCytokinesGastroenterologyInflammationPharmacology

Identifiers

PMID36166295
PMCPMC9675483
OpenAlexW4297253276

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.