Pancreatic Stellate Cells (PSCs) are specialized cells residing in the pancreas with crucial roles in tissue repair, fibrosis, and inflammation. Originally identified for their role in storing vitamin A in lipid droplets, PSCs are activated in response to injury or inflammation, contributing to the pathophysiology of pancreatic diseases. Upon activation, PSCs undergo a transformation into myofibroblast-like cells, promoting the synthesis and deposition of extracellular matrix proteins, such as collagen. This process is a hallmark of pancreatic fibrosis, a common feature in conditions like chronic pancreatitis and pancreatic cancer. Excessive activation and proliferation of PSCs can lead to the formation of a fibrotic, scar-like tissue, impairing pancreatic function. Research on PSCs aims to understand the molecular mechanisms governing their activation and function. Various signaling pathways, including transforming growth factor-beta (TGF-β) and platelet-derived growth factor (PDGF), play key roles in PSC activation. Targeting these pathways is a focus of therapeutic strategies to mitigate fibrosis and improve outcomes in pancreatic diseases. The role of PSCs extends beyond fibrosis, as they also influence the tumor microenvironment in pancreatic cancer. PSCs interact with cancer cells, promoting tumor growth, invasion, and resistance to treatment. Targeting PSCs in cancer therapy is an active area of investigation to enhance the efficacy of anti-cancer treatments. Understanding the complex interplay between PSCs, immune cells, and other cell types in the pancreas is crucial for developing targeted therapies. Emerging research explores the potential of modulating PSC activity to prevent or reverse fibrosis, enhance drug delivery, and improve the overall prognosis of pancreatic diseases. In summary, pancreatic stellate cells play a pivotal role in pancreatic fibrosis and the tumor microenvironment in pancreatic cancer. Investigating their activation mechanisms and interactions with other cell types is essential for developing therapeutic strategies to address fibrosis and improve outcomes in pancreatic diseases.
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Title :
Nagy Habib, Imperial College London, United Kingdom
Title :
Alexander Seifalian, Nanotechnology & Regenerative Medicine Commercialisation Centre, United Kingdom
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