Pharmacological exploration of novel molecular mechanisms in experimental chronic pancreatitis Emphasis on SIRT1 AMPK and DDR Pathways

Abstract

Chronic pancreatitis (CP) is the persistent inflammatory condition arise from repetitive episodes of AP, where dysregulation of the secretion and premature activation of pancreatic enzymes results in exocrine and endocrine pancreatic damage, subsequently results in severe maldigestion and diabetes. The incidence and prevalence of CP is higher than that of AP. CP is characterized by chronic abdominal pain accompanied with progressive and irreversible dysfunction of exocrine and endocrine pancreas which ultimately leads to the permanent damage of the pancreatic functions. CP also a major risk factor for the development of the diabetes and pancreatic cancer. Pathologically, CP is characterized by permanent destruction of acinar cells, inflammatory cell infiltration, and collagen deposition.Although, SIRT1, AMPK and collagen receptors DDR1 and DDR2 play crucial role in inflammatory and fibrotic diseases, but their role in CP are not explored yet. Therefore, in the current thesis work, we aimed to explore the potential molecular targets in CP newline