Bidirectional regulation of pancreatic stellate cell-mediated pancreatic fibrosis by prostaglandin subtypes: mechanisms and therapeutic implications
- 1College of Basic Medicine, Naval Medical University, Shanghai, 200433 China
- 2Department of Traditional Chinese Medicine, Naval Hospital of Eastern Theater, Zhoushan, 316000 China
- 3Department of Traditional Chinese Medicine, Naval Medical University, Shanghai, 200433 China
Abstract
Chronic pancreatitis (CP) is a recurrent inflammatory pancreatic disease characterized by progressive parenchymal damage. Currently, there are no effective clinical approaches to halt pancreatic fibrosis progression. As a core mediator involved in inflammation and fibrogenesis, prostaglandin (PG) participates in diverse inflammatory signaling cascades via the arachidonic acid metabolic pathway and further modulates pancreatic stellate cell (PSC) activation and extracellular matrix (ECM) deposition. This review systematically summarizes how distinct PG subtypes bind to corresponding receptors to regulate multiple signaling pathways and mediate PSC-related pancreatic fibrosis. It offers novel insights into developing targeted drugs against PG-related pathways and optimizing clinical treatment strategies for pancreatic fibrosis.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s11033-026-12993-3.
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BibTeX
@article{wang2026bidirectional,
title = {{Bidirectional regulation of pancreatic stellate cell-mediated pancreatic fibrosis by prostaglandin subtypes: mechanisms and therapeutic implications}},
author = {Sichun Wang and Hubo Chen and Lina Wang},
journal = {Molecular Biology Reports},
year = {2026},
month = nov,
doi = {10.1007/s11033-026-12993-3},
url = {https://doi.org/10.1007/s11033-026-12993-3},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Bidirectional regulation of pancreatic stellate cell-mediated pancreatic fibrosis by prostaglandin subtypes: mechanisms and therapeutic implications
AU - Sichun Wang
AU - Hubo Chen
AU - Lina Wang
PY - 2026
DA - 2026/11/04
JO - Molecular Biology Reports
DO - 10.1007/s11033-026-12993-3
UR - https://doi.org/10.1007/s11033-026-12993-3
AB - Chronic pancreatitis (CP) is a recurrent inflammatory pancreatic disease characterized by progressive parenchymal damage. Currently, there are no effective clinical approaches to halt pancreatic fibrosis progression. As a core mediator involved in inflammation and fibrogenesis, prostaglandin (PG) participates in diverse inflammatory signaling cascades via the arachidonic acid metabolic pathway and further modulates pancreatic stellate cell (PSC) activation and extracellular matrix (ECM) deposition. This review systematically summarizes how distinct PG subtypes bind to corresponding receptors to regulate multiple signaling pathways and mediate PSC-related pancreatic fibrosis. It offers novel insights into developing targeted drugs against PG-related pathways and optimizing clinical treatment strategies for pancreatic fibrosis. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s11033-026-12993-3.
SN - 0301-4851
SN - 1573-4978
ER -