Acute pancreatitis (ap) is a serious inflammatory disease, and its pathogenesis is not yet fully elucidated. So, there is no specific treatment for AP in clinical practice. More and more studies have demonstrated that mitochondrial injury is at the center of the pathogenesis of AP. It is currently considered that mitochondrial injury is closely associated with calcium overload, intracellular ATP depletion, changes in mitochondrial membrane permeability, and impaired autophagy. These pathological changes are jointly involved in the occurrence and development of AP. In addition, the regulation of mitochondria on the death pathway of acinar cells also exerts important roles in AP. Here, the authors address the research progress of the pathological mechanism of mitochondrial dysfunction in AP.