Pancreatitis is a common disorder with significant morbidity and mortality, yet little is known about its pathogenesis, and there is no specific or effective treatment. Its development involves dysregulated autophagy and unresolved inflammation, demonstrated by studies in genetic and experimental mouse models. Disease severity depends on whether the inflammatory response resolves or amplifies, leading to multi-organ failure. Dysregulated autophagy might promote the inflammatory response in the pancreas. We discuss the roles of autophagy and inflammation in pancreatitis, mechanisms of deregulation, and connections among disordered pathways. We identify gaps in our knowledge and delineate perspective directions for research. Elucidation of pathogenic mechanisms could lead to new targets for treating or reducing the severity of pancreatitis.

胰腺炎是一种常见疾病，发病率和死亡率很高，但对其发病机制知之甚少，也没有特异性或有效的治疗方法。遗传和实验小鼠模型的研究证明，其发展涉及自噬失调和未解决的炎症。疾病的严重程度取决于炎症反应是否消退或放大，从而导致多器官衰竭。自噬失调可能会促进胰腺的炎症反应。我们讨论了自噬和炎症在胰腺炎中的作用、失调机制以及紊乱途径之间的联系。我们找出知识差距并描绘研究的前景方向。阐明致病机制可能会产生治疗胰腺炎或减轻胰腺炎严重程度的新目标。