Advancements in Understanding the Interplay between Mitophagy and Acute Pancreatitis: A Comprehensive Research Overview

Acute pancreatitis (AP) is characterized by the abnormal activation of pancreatic enzymes within the pancreas, triggering inflammatory responses such as auto-digestion and necrosis of tissue. As a prevalent clinical condition, AP manifests with symptoms including abdominal pain, nausea, and fever, and in severe cases can be fatal. Despite its prevalence, the etiology of AP is complex, with an unknown cause and a scarcity of effective treatments. Possible triggers for AP include bile duct obstruction from gallstones, prolonged and excessive alcohol consumption, pancreatic vascular embolism, infection, and dysfunction. A noteworthy contributor to AP is the dysfunction of pancreatic cells induced by mitochondrial autophagy, an increasingly prominent focus of research in this field. Inflammatory vesicles, reactive oxygen radicals, endoplasmic reticulum stress, calcium overload, and iron-induced death are intricately linked to both mitochondrial autophagy and AP. This review consolidates insights into the pathogenesis of mitochondrial autophagy and AP, offering novel perspectives and avenues for the diagnosis and treatment of AP.