Evidence map›Paper›PMID 31506423›Full record

ArticleCell death & disease2019

ATF6 regulates the development of chronic pancreatitis by inducing p53-mediated apoptosis.

Lei Zhou, Jie-Hui Tan, Rong-Chang Cao, Jia Xu, Xue-Mei Chen, Zhao-Chang Qi, Su-Ying Zhou, Su-Bing Li, Qi-Xin Mo, Zhi-Wei Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. 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
8.6field-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, 50 citations in OpenAlex.

  1. Article
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  3. International journal of molecular sciences · 2026
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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

11 authors at 2 institutions in 1 country.

Lei ZhouDepartment of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jie-Hui TanDepartment of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Rong-Chang CaoDepartment of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jia XuDepartment of Pathophysiology, Southern Medical University, Guangzhou, 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.
Zhao-Chang QiThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Su-Ying ZhouThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Su-Bing LiThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Qi-Xin MoThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Zhi-Wei LiThe First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Guo-Wei ZhangDepartment of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China. guoweizhang77@163.com.
Southern Medical University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic pancreatitis (CP) is a progressive, recurrent inflammatory disorder of the pancreas. Initiation and progression of CP can result from serine protease 1 (PRSS1) overaccumulation and the ensuing endoplasmic reticulum (ER) stress. However, how ER stress pathways regulate the development and progression of CP remains poorly understood. In the present study we aimed to elucidate the ER stress pathway involved in CP. We found high expression of the ER stress marker genes ATF6, XBP1, and CHOP in human clinical specimens. A humanized PRSS1 transgenic mouse was established and treated with caerulein to mimic the development of CP, as evidenced by pathogenic alterations, collagen deposition, and increased expression of the inflammatory factors IL-6, IL-1β, and TNF-α. ATF6, XBP1, and CHOP expression levels were also increased during CP development in this model. Acinar cell apoptosis was also significantly increased, accompanied by upregulated p53 expression. Inhibition of ATF6 or p53 suppressed the expression of inflammatory factors and progression of CP in the mouse model. Finally, we showed that p53 expression could be regulated by the ATF6/XBP1/CHOP axis to promote the development of CP. We therefore conclude that ATF6 signalling regulates CP progression by modulating pancreatic acinar cell apoptosis, which provides a target for ER stress-based diagnosis and treatment of CP.

Indexed as

ApoptosisGene Expression RegulationSignal TransductionActivating Transcription Factor 6AdolescentAdultAgedAnimalsEndoplasmic Reticulum StressFemaleHumansMaleMiceMiddle AgedPancreatitis, ChronicTumor Suppressor Protein p53Activating Transcription Factor 6ATF6 protein, humanAtf6 protein, mouseTP53 protein, humanTrp53 protein, mouseTumor Suppressor Protein p53

Identifiers

PMID31506423
PMCPMC6737032
OpenAlexW2972955757

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.