Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Pancreatic acinar cells exhibit a remarkable polarization of Ca2+ release and Ca2+ influx mechanisms. In the present brief review, we discuss the localization of channels responsible for Ca2+ release [mainly IP3 (inositol 1,4,5-trisphosphate) receptors] and proteins responsible for SOCE (store-operated Ca2+ entry). We also place these Ca2+-transporting mechanisms on the map of cellular organelles in pancreatic acinar cells, and discuss the physiological implications of the cellular geography of Ca2+ signalling. Finally, we highlight some unresolved questions stemming from recent observations of co-localization and co-immunoprecipitation of IP3 receptors with Orai channels in the apical (secretory) region of pancreatic acinar cells.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1042/BST20110639 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
HMGB1 contributes to pancreatic fibrosis by regulating TLR4-mediated autophagy and the NLRP3 inflammasome pathway in chronic pancreatitis.
Exp Cell Res
September 2025
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, 300100, China; Institute of Integrative Medicine for Acute Abdominal Diseases, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin 300100,
The characteristic pathological change in chronic pancreatitis (CP) is pancreatic fibrosis. In the early stages of CP development, injured acinar cells induce the infiltration of inflammatory cells, followed by pancreatic stellate cell (PSC) activation. Activated PSC induce the deposition of extracellular matrix (ECM) and promote the development of pancreatic fibrosis.
View Article and Find Full Text PDFLiquiritigenin Alleviates Inflammation and Mitochondrial Dysfunction in Acute Pancreatitis via ERβ-VDAC1 Signaling.
J Ethnopharmacol
September 2025
Department of Emergency Medicine, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610072, China. Electronic address:
Ethnopharmacological Relevance: Liquorice (Gancao), a classic Chinese herb, has been historically prescribed for inflammation and gastrointestinal disorders. Its bioactive flavonoid liquiritigenin (4',7-dihydroxyflavone) exhibits anti-inflammatory properties, yet its efficacy against acute pancreatitis (AP) remains unexplored.
Aim: To systematically investigate the therapeutic potential of liquiritigenin against AP and decipher its estrogen receptor beta (ERβ)-mediated mitochondrial regulatory mechanisms.
A redundant system of thioredoxin and glutathione is essential for pancreatic acinar integrity.
Cell Mol Gastroenterol Hepatol
September 2025
Department of Medicine II, Klinikum rechts der Isar, School of Medicine, Technical University of Munich, Munich, Germany. Electronic address:
Background & Aims: Oxidative stress and antioxidant defense mechanisms have long been implicated in the pathogenesis of acute pancreatitis (AP). However, there is a notable lack of in vivo experimental evidence clarifying their precise role.
Methods: We generated and analyzed mice with a pancreas-specific deletion of Txnrd1 (Txnrd1).
TRPV6-mediated store-operated Ca entry participates in pancreatic acinar cell injury during acute pancreatitis.
Cell Mol Gastroenterol Hepatol
September 2025
West China Centre of Excellence for Pancreatitis, Institute of Integrated Traditional Chinese and Western Medicine, West China Hospital, Sichuan University, Chengdu, China. Electronic address:
Background & Aims: Suppressing toxic Ca accumulation in pancreatic acinar cells (PACs) is the central therapeutic strategy of acute pancreatitis (AP). Store-operated Ca entry (SOCE) represents an important mechanism promoting Ca overload, which remains incompletely understood in AP. Transient receptor potential vanilloid 6 (TRPV6) is an ion channel highly selective to Ca, and its role in PACs or AP onset remains largely unknown.
View Article and Find Full Text PDFDeubiquitinase JOSD2 promotes acute pancreatitis by removing K63-linked poly-ubiqutin chain on PCNA in pancreatic acinar cells.
Cell Mol Gastroenterol Hepatol
September 2025
Medical Research Center, the First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China; School of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China. Electronic address:
Background & Aims: Acute pancreatitis (AP) results in localized pancreatic injury or systemic inflammatory responses, contributing to high morbidity and mortality worldwide. Acinar cell death and inflammation are critical key drivers of AP progression. Some deubiquitinases (DUBs), which regulate the stability and/or activity of substrate proteins, may play a role in the development of AP.
View Article and Find Full Text PDF