Evidence map›Paper›PMID 42029961›Full record

ArticleDigestive diseases and sciences2026

Development of a Novel Mouse Model of Severe Acute Pancreatitis with Pathological Features Recapitulating Human Disease.

Qin Qin, Dujiang Yang, Mao Wang, Yiran Song, Simeng Tan, Hanzhang Wang, Yu Zou, Yuchuan Deng, Huimin Lu, Yu Zheng

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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.

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2 · The registry

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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

1 citing paper in PubMed.

  1. Article
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

10 authors.

Qin Qin *Department of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 17, 3Rd Section, Renmin Nan Rd, Chengdu, China.
Dujiang Yang *Division of Pancreatic Surgery, Department of General Surgery, West China Hospital, Sichuan University, No. 37, Guoxue Alley, Chengdu, 610041, Sichuan Province, China.
Mao WangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 17, 3Rd Section, Renmin Nan Rd, Chengdu, China.
Yiran SongDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 17, 3Rd Section, Renmin Nan Rd, Chengdu, China.
Simeng TanDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 17, 3Rd Section, Renmin Nan Rd, Chengdu, China.
Hanzhang WangDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 17, 3Rd Section, Renmin Nan Rd, Chengdu, China.
Yu ZouDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 17, 3Rd Section, Renmin Nan Rd, Chengdu, China.
Yuchuan DengDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 17, 3Rd Section, Renmin Nan Rd, Chengdu, China.
Huimin LuCenter of Excellence for Pancreatitis, Institute of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China. hm.lu@scu.edu.cn.
Yu ZhengDepartment of Biotherapy, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, No. 17, 3Rd Section, Renmin Nan Rd, Chengdu, China. zhengyu82@scu.edu.cn.

Funding

Natural Science Foundation of Sichuan Province 2024NSFSC0606Natural Science Foundation of Sichuan Province 2024YFHZ0053
6 · The paper itself

Abstract

backgroundCurrent severe acute pancreatitis (SAP) murine models face significant limitations. The sodium taurocholate method consistently induces pancreatic necrosis but demands intricate surgical procedures, leading to high variability and infection risks. In contrast, the arginine approach causes acinar cell damage without fully mimicking clinical injury pathways. Furthermore, the caerulein-lipopolysaccharide (CAE-LPS) model, while operationally straightforward, fails to replicate persistent organ failure due to LPS's rapid clearance, thereby inadequately capturing the lethal trajectory observed in clinical SAP patients who succumb to the disease.

aimsTo address these gaps, we developed a SAP mouse model by integrating two key pathogenic mechanisms: trypsin-driven complement activation and sustained complement hyperactivation as drivers of multiple organ failure.

methodsThe SAP model was established by combining CAE-induced pancreatic injury with zymosan (ZYM)-mediated complement activation. Dosing and combination protocols were meticulously optimized and were followed by a comprehensive longitudinal analysis during the acute phase (0-12 days), with comparisons to the CAE-LPS model.

resultsThe optimized protocol involved nine intraperitoneal CAE injections (100 μg/kg each) followed by a single ZYM dose (1000 mg/kg). This regimen triggered pancreatic necrosis, inflammatory infiltration, and multi-organ damage (liver, kidney, intestine). Notably, the model demonstrated sustained complement activation and a mortality pattern in non-survivors that more closely aligned with clinical SAP outcomes than the CAE-LPS model.

conclusionThis novel model offers a robust platform for advancing SAP research, bridging the divide between preclinical studies and clinical translation.

Indexed as

Disease Models, AnimalPancreasPancreatitisAcute DiseaseAnimalsCeruletideComplement ActivationHumansLipopolysaccharidesMaleMiceMice, Inbred C57BLMultiple Organ FailureZymosanCeruletideLipopolysaccharidesZymosanCaeruleinComplement cascadeLPSMulti-organ failureServe acute pancreatitisZymosan

Identifiers

PMID42029961

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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.