Evidence map›Paper›PMID 31974911›Full record

ArticleDigestive diseases and sciences2020

P53 Activated by ER Stress Aggravates Caerulein-Induced Acute Pancreatitis Progression by Inducing Acinar Cell Apoptosis.

Lei Zhou, Jie-Hui Tan, Wan-Yan Zhou, Jia Xu, Shi-Jing Ren, Zhen-Yu Lin, Xue-Mei Chen, Guo-Wei Zhang

Abstract read
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In one paragraph

Article in Digestive diseases and sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

11 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Acute pancreatitis: mechanisms and therapeutic approaches.Signal transduction and targeted therapy · 2026
    Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Fic-mediated AMPylation tempers the unfolded protein response during physiological stress.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Article
  9. Article
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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

8 authors at 2 institutions in 1 country.

Lei ZhouDivision of Hepatobiliopancreatic Surgery, Department of General Surgery, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, People's Republic of China.
Jie-Hui TanDivision of Hepatobiliopancreatic Surgery, Department of General Surgery, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, People's Republic of China.
Wan-Yan ZhouDepartment of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jia XuDepartment of Pathophysiology, Southern Medical University, Guangzhou, China.
Shi-Jing RenDepartment of Endocrinology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhen-Yu LinDivision of Hepatobiliopancreatic Surgery, Department of General Surgery, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, People's Republic of China.
Xue-Mei ChenDepartment of Occupational Health and Medicine, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou, China.
Guo-Wei ZhangDivision of Hepatobiliopancreatic Surgery, Department of General Surgery, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, People's Republic of China. guoweizhang77@163.com.ORCID 0000-0002-1487-6340
Nanfang Hospital · CNSouthern Medical University · CN

Funding

Clinical Research Program of Nanfang Hospital, Southern Medical University 2018CR046Clinical Research Startup Program of Southern Medical University by High-level University Construction Funding of Guangdong Provincial Department of Education LC2016PY011Science and Technology Planning Project of Guangdong Province 2019A030317018Scientific Research Startup Program of Southern Medical University by High-level University Construction Funding of Guangdong Provincial Department of Education CX2018N012
6 · The paper itself

Abstract

BACKGROUND AND

aimsAcute pancreatitis (AP) is a severe pancreatic disorder that remains associated with high mortality due to a lack of effective drugs and management strategies. This study aimed to investigate the molecular pathogenic mechanisms of AP involving p53 and endoplasmic reticulum (ER) stress pathways.

methodsExpression of PRSS1 and p53 in human AP tissues was detected by immunohistochemistry and Western blotting. AP was induced with caerulein in humanized PRSS1 transgenic mice, and its severity was verified by histological imaging, evaluation of edema, serum amylase, and trypsin activity assays. A transferase-mediated d-UTP nick end-labeling assay was performed to evaluate acinar cell apoptosis associated with AP. The expression of ER stress genes was assessed by quantitative RT-PCR (qRT-PCR) and Western blotting.

resultsPRSS1 and p53 were highly expressed in human AP tissues. Expression of human PRSS1 in caerulein-treated mice induced significant acinar cell apoptosis and AP progression. P53 knockout significantly suppressed AP progression in humanized PRSS1 transgenic mice. The ER stress pathway was activated by PRSS1 and mediated the progression of AP in mouse pancreatic tissues. Application of a p53 inhibitor effectively ameliorated caerulein-induced AP in PRSS1 transgenic mice, while a p53 activator promoted the progression of AP.

conclusionP53, which was activated by the ER stress pathway, promoted the progression of AP in mice expressing PRSS1 by inducing acinar cell apoptosis.

Indexed as

Acinar CellsAnimalsApoptosisCeruletideEndoplasmic Reticulum StressHumansMiceMice, TransgenicPancreatitisTrypsinTumor Suppressor Protein p53CeruletidePRSS1 protein, humanPrss1 protein, mouseTrypsinTumor Suppressor Protein p53Acute pancreatitisApoptosisER stressP53PRSS1

Identifiers

PMID31974911
OpenAlexW3002503101

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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.