Research progress of iron death and autophagy in acute pancreatitis
Acute pancreatitis (AP) is a common and potentially life-threatening inflammatory disorder of the pancreas. Although it is typically self-limiting,up to 20％ of patients may progress to severe acute pancreatitis (SAP),which can lead to systemic inflammatory response syndrome (SIRS),multiple organ dysfunction and failure,affecting organs such as the lungs,kidneys,liver,and heart. Survivors often experience varying degrees of sequelae,including post-pancreatitis diabetes,exocrine pancreatic insufficiency,and chronic pancreatitis. Currently,the primary treatment approaches involve fluid resuscitation and a series of supportive therapies. This low-targeted treatment strategy is a major reason for the persistently high mortality rates associated with AP,particularly SAP. Previous studies have indicated that calcium ions can mediate acinar cell damage and death,as well as influence the unfolded protein response and autophagy,affecting the pathogenesis of pancreatitis. However,our understanding of the mechanisms of acinar parenchymal cell death and other pathogenic factors remains limited,leading to a symptomatic and supportive stage of treatment for AP. Iron death and autophagy are distinct mechanisms of regulated cell death. Iron death is a novel form of cell death triggered by iron-dependent lipid peroxidation,while autophagy is the primary catabolic process through which cells eliminate damaged,defective,or unwanted organelles,along with long-lived proteins and lipids,recycling their components to meet energy demands and biogenetic needs. Both mechanisms have unique characteristics and are interconnected,playing significant roles in AP. This article reviews recent advances in the research on iron death and autophagy in the pathogenesis of AP,providing new insights and regulatory targets for understanding and treating AP,which may facilitate the development of more effective targeted therapies.
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