ArticleThe Journal of biological chemistry2014
Endoplasmic reticulum stress is chronically activated in chronic pancreatitis.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.
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Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.
- TRPV6, a new entrant as a susceptibility gene in chronic pancreatitis: evidence from a systematic review and meta-analysis.BMC gastroenterology · 2026Pooled it
- Loss of the ER-cargo protein CLN8 increases severity of acute pancreatitis and upregulates ER-stress and ER-phagy.Molecular biomedicine · 2026Article
- The Stathmin 1-lineage Contributes to Acinar Regeneration but Not to Neoplasia Upon Oncogenic Kras Expression.Cellular and molecular gastroenterology and hepatology · 2026Article
- Nanotherapy for Pancreatitis: From Single-Cell Targeting Toward Multicellular-Coordinated Regulation.International journal of nanomedicine · 2026Review
- From single-pathway cascade to network pathophysiology: how genetically engineered mouse models reshaped our understanding of pancreatitis.Frontiers in physiology · 2026Review
- Acinar-specific loss of activating transcription factor 3 restricts KRASCell death discovery · 2025Article
- Ubiquitin-specific protease 7 exacerbates acute pancreatitis progression by enhancing ATF4-mediated autophagy.In vitro cellular & developmental biology. Animal · 2025Article
- Lysine acetylation and its role in the pathophysiology of acute pancreatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- The Effects of Da-Chai-Hu Decoction Alleviating Pancreatic Exocrine Dysfunction by Inhibiting Endoplasmic Reticulum Stress of Acinar Cell in Mice with Chronic Pancreatitis.Journal of inflammation research · 2025Article
- The Integrated Stress Response in Pancreatic Development, Tissue Homeostasis, and Cancer.Gastroenterology · 2024Review
- Analysis of risk factors related to acute exacerbation in patients with chronic pancreatitis: a retrospective study of 313 cases from a single center in China.BMC gastroenterology · 2024Article
- Genetic knock-in of EIF2AK3 variants reveals differences in PERK activity in mouse liver and pancreas under endoplasmic reticulum stress.Scientific reports · 2024Article
- Western diet-induced ultrastructural changes in mouse pancreatic acinar cells.Frontiers in cell and developmental biology · 2024Article
- NFIC regulates ribosomal biology and ER stress in pancreatic acinar cells and restrains PDAC initiation.Nature communications · 2023Article
- Altered MANF Expression in Pancreatic Acinar and Ductal Cells in Chronic Alcoholic Pancreatitis: A Cross-Sectional Study.Biomedicines · 2023Article
- Effects of Berberine against Pancreatitis and Pancreatic Cancer.Molecules (Basel, Switzerland) · 2022Review
- A multi-omics approach identifies pancreatic cancer cell extracellular vesicles as mediators of the unfolded protein response in normal pancreatic epithelial cells.Journal of extracellular vesicles · 2022Article
- New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice.Journal of veterinary internal medicine · 2022Review
- Misfolding-induced chronic pancreatitis in CPA1 N256K mutant mice is unaffected by global deletion of Ddit3/Chop.Scientific reports · 2022Article
- Exposure to binge ethanol and fatty acid ethyl esters exacerbates chronic ethanol-induced pancreatic injury in hepatic alcohol dehydrogenase-deficient deer mice.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The pathogenesis of chronic pancreatitis (CP) is poorly understood. Endoplasmic reticulum (ER) stress has now been recognized as a pathogenic event in many chronic diseases. However, ER stress has not been studied in CP, although pancreatic acinar cells seem to be especially vulnerable to ER dysfunction because of their dependence on high ER volume and functionality. Here, we aim to investigate ER stress in CP, study its pathogenesis in relation to trypsinogen activation (widely regarded as the key event of pancreatitis), and explore its mechanism, time course, and downstream consequences during pancreatic injury. CP was induced in mice by repeated episodes of acute pancreatitis (AP) based on caerulein hyperstimulation. ER stress leads to activation of unfolded protein response components that were measured in CP and AP. We show sustained up-regulation of unfolded protein response components ATF4, CHOP, GRP78, and XBP1 in CP. Overexpression of GRP78 and ATF4 in human CP confirmed the experimental findings. We used novel trypsinogen-7 knock-out mice (T(-/-)), which lack intra-acinar trypsinogen activation, to clarify the relationship of ER stress to intra-acinar trypsinogen activation in pancreatic injury. Comparable activation of ER stress was seen in wild type and T(-/-) mice. Induction of ER stress occurred through pathologic calcium signaling very early in the course of pancreatic injury. Our results establish that ER stress is chronically activated in CP and is induced early in pancreatic injury through pathologic calcium signaling independent of trypsinogen activation. ER stress may be an important pathogenic mechanism in pancreatitis that needs to be explored in future studies.
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Registered trials
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.