Smoking Is Related to Pancreatic Fibrosis in Humans

2011 ◽  
Vol 106 (6) ◽  
pp. 1161-1166 ◽  
Author(s):  
Erwin J M van Geenen ◽  
Mark M Smits ◽  
Tim C M A Schreuder ◽  
Donald L van der Peet ◽  
Elisabeth Bloemena ◽  
...  
Keyword(s):  
Pancreatic Fibrosis

Effect of antioxidant on cerulein-induced pancreatic fibrosis; in vitro and in vivo effect

2001 ◽  
Vol 120 (5) ◽  
pp. A721-A721
Author(s):  
T OH ◽  
B YOO ◽  
K KO ◽  
B AHN ◽  
H CHO ◽  
...  
Keyword(s):  
Pancreatic Fibrosis

Pancreatic fibrosis in chronic pancreatitis: A new approach of non-invasive diagnosis in clinic

Pancreatology ◽  
2021 ◽  
Vol 21 ◽  
pp. S89-S90
Author(s):  
K. Lesko ◽  
G. Varvanina ◽  
D. Bordin ◽  
E. Dubtsova ◽  
M. Malykh ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Pancreatic Fibrosis ◽  
New Approach ◽  
Non Invasive

Pancreatic fibrosis and standard diagnostics

2015 ◽  
Vol 12 (2) ◽  
pp. 68-70 ◽  
Author(s):  
Güralp O. Ceyhan ◽  
Helmut Friess
Keyword(s):  
Pancreatic Fibrosis

Activated Pancreatic Stellate Cells Promote Acinar Duct Metaplasia by Disrupting Mitochondrial Respiration and Releasing Reactive Oxygen Species

2021 ◽  
Vol 01 ◽  
Author(s):  
Hong Xiang ◽  
Fangyue Guo ◽  
Qi Zhou ◽  
Xufeng Tao ◽  
Deshi Dong
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Respiration ◽  
Reactive Oxygen ◽  
Acinar Cells ◽  
Stellate Cells ◽  
Pancreatic Fibrosis ◽  
Pancreatic Stellate Cells ◽  
Pancreatic Acinar Cells ◽  
Oxygen Species

Background: Chronic pancreatitis (CP) is a long-term risk factor for pancreatic ductal adenocarcinoma (PDAC), and both diseases share a common etiology. The activation of Pancreatic stellate cells (PaSCs) caused by inflammation of the chronic pancreas plays a pivotal role in the pathology of pancreatic fibrosis and the malignant phenotype of PDAC. However, the central role of activated PaSCs in acinar-to-ductal metaplasia (ADM) remains unknown. Objective: In the present study, we investigated the link between pancreatic fibrosis and ADM and the possible underlying mechanism. Methods: A caerulein-treated mouse CP model was established, and Masson trichrome histochemical stain and transmission electron microscope (TEM) were used to observe stromal fibrosis and cell ultrastructure, respectively. The expression of amylase and cytokeratin 19 (CK19), mitochondria respiration, and reactive oxygen species (ROS) were detected in vitro in the co-culture model of primary pancreatic acinar cells and PaSCs. Results: The activation of PaSCs and pancreatic fibrosis were accompanied by ADM in pancreatic parenchyma in caerulein-treated mice, which was verified by the co-cultivation experiment in vitro. Furthermore, we showed that activated PaSCs promote ADM by disrupting mitochondrial respiration and releasing ROS. The expression of inflammation-and ADM-related genes, including S100A8, S100A9, and CK19, was observed to be up-regulated in pancreatic acinar cells in the presence of activated PaSCs. The expression of S100A9 and CK19 proteins was also up-regulated in acinar cells co-cultured with activated PaSCs. Conclusion: The manipulation of mitochondrial respiration and ROS release is a promising preventive and/or therapeutic strategy for PDAC, and S100A9 is expected to be a therapeutic target to block the ADM process induced by the activation of PaSCs.

scholarly journals Aetiology of Chronic Pancreatic Fibrosis with Calcification Seen in Uganda

BMJ ◽  
1964 ◽  
Vol 1 (5398) ◽  
pp. 1607-1609 ◽  
Author(s):  
A. G. Shaper
Keyword(s):  
Pancreatic Fibrosis
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