Abstract
Pancreatitis and alcoholic pancreatitis are serious health concerns with an urgent need for effective treatment strategies. Alcohol is a known etiological factor for pancreatitis, including acute pancreatitis (AP) and chronic pancreatitis (CP). Excessive alcohol consumption induces many pathological stress responses; of particular note is endoplasmic reticulum (ER) stress and adaptive unfolded protein response (UPR). ER stress results from the accumulation of unfolded/misfolded protein in the ER and is implicated in the pathogenesis of alcoholic pancreatitis. Here, we summarize the possible mechanisms by which ER stress contributes to alcoholic pancreatitis. We also discuss potential approaches targeting ER stress and UPR in developing novel therapeutic strategies for the disease.
Highlights
In a genome-wide study, a CLDN2 risk allele, which is associated with an abnormal expression of CLDN2 protein in pancreatic acinar cells, was identified as a risk factor that interacted with alcohol consumption to accelerate the progression of chronic pancreatitis [62]
Using an in vitro model, we showed that an siRNA knockdown of mesencephalic astrocyte-derived neurotrophic factor (MANF) exacerbated alcohol-induced damages in mouse pancreatic 266-6 acinar cells in which the addition of recombinant human MANF
Pancreatitis remains a serious medical concern worldwide, with no FDAapproved drugs or treatments available for the disease. Both acute pancreatitis (AP) and chronic pancreatitis (CP) are commonly caused by excessive alcohol use along with other risk factors, including smoking, high-fat diet and genetic mutations
Summary
Pancreatitis is a common inflammatory disorder of the pancreas, associated with high mortality and healthcare burdens worldwide [1,2]. It mainly consists of two forms: acute pancreatitis (AP) and chronic pancreatitis (CP). One quarter to one third of AP patients develop EPI during the follow-up period [13,14]. The prevalence of EPI following AP is higher with the severe form than with the mild form, and it is higher in patients with an etiology of alcohol than one of gallstones [14]. The high disease burden of AP and CP emphasizes the importance of identifying predisposing factors, understanding pathogenesis, and developing therapeutic intervention for these diseases
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