A New Frontier in Pancreatic Fibrosis Therapy

By targeting cellular fibrosis pathways and inflammatory signaling, our approach offers a powerful new strategy to reverse damage and restore pancreatic integrity

Pancreatic Fibrosis

Pancreatic fibrosis, a hallmark of chronic pancreatitis, increased globally from 1.73 million cases in 1990 to 2.75 million in 2021, a 59% rise. Risk factors include chronic alcohol consumption, smoking, hypertriglyceridemia, type 2 diabetes, and gallstones. This fibrotic response impairs both exocrine and endocrine functions, significantly affecting quality of life. Activated pancreatic stellate cells (PSCs) promote ECM (Extra Cellular Matrix) production and cytokine secretion, exacerbating inflammation and destroying acinar and islet cells. As damage progresses, functional tissue is replaced by fibrotic material, leading to irreversible loss of function. Currently, there are no effective USFDA-approved therapies specifically targeting the reversal of pancreatic tissue damage caused by chronic pancreatitis. The accumulation of ECM components such as type I collagen, fibronectin, and periostin is central to the fibrosis, altering the cellular microenvironment and contributing to disease progression.

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