AI Article Synopsis

  • Chronic pancreatitis involves progressive inflammation of the pancreas leading to irreversible damage due to fibrosis, often triggered by alcohol consumption, though its exact molecular causes remain unclear.
  • Recent research highlights oxidative stress as a key factor in activating pancreatic stellate cells, which contributes to collagen deposition and fibrogenesis.
  • The review explores the impact of oxidative stress on pancreatic fibrosis, discusses molecular pathways for protecting cells from damage, and evaluates potential antioxidative treatments, including dimethyl fumarate, which may help reduce fibrogenesis by inhibiting pancreatic stellate cell activation.

Article Abstract

Chronic pancreatitis is the progressive inflammation of the pancreas resulting in the irreversible damage of pancreatic structure and function by means of fibrosis. Chronic pancreatitis is most commonly caused by alcohol consumption, although the direct molecular etiology is unknown. Recent studies suggest oxidative stress as a catalyst for pancreatic stellate cell activation leading to the deposition of collagenous extracellular matrix causing pancreatic fibrosis. We review the effect of oxidative stress on pancreatic fibrogenesis and indicate the molecular pathways involved in preventing oxidant-related cell damage. Likewise, we summarize existing antioxidative therapies for chronic pancreatitis and discuss a novel nuclear factor erythroid 2-related factor 2 activator, dimethyl fumarate, and its potential to reduce fibrogenesis by downregulating pancreatic stellate cell activation.

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Source
http://dx.doi.org/10.1097/MPA.0000000000001433DOI Listing

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