腺泡细胞自噬与急性胰腺炎

Autophagy in pancreatic acinar cells and pathogenesis of acute pancreatitis

急性胰腺炎(acute pancreatitis,AP)是胰腺外分泌急性炎症的疾病,其发病机制至今尚未阐明.胰腺腺泡细胞内酶原激活是公认的AP发病的始动环节,越来越多的证据表明,异常自噬酶原激活将导致腺泡细胞损伤和AP.腺泡细胞在病理因素的刺激下发生线粒体通透性转换,线粒体去极化和ATP下降,可导致细胞内胰酶活性升高和细胞坏死.我们认为,阐明线粒体通透性转换与自噬二者之间的关系及腺泡细胞自噬在AP中的作用,将有望推进对AP发病机制的认识,为AP的有效防治提供新思路和药物作用新靶点.

Acute pancreatitis is an inflammatory disorder of the pancreas, and its pathogenesis remains poorly understood. Autodigestion of the pancreas by its own prematurely activated digestive proteases is a critical event in the onset of acute pancreatitis. Mitochondrial permeability transition results in mitochondrial depolarization and loss of ATP production, which has been found to induce autophagy in several cell types, e.g.cardiomyocytes and hepatocytes and is of vital importance for the fate of cells. Elucidating the relationship between mitochondrial permeability transition and autophagy within pancreatic acinar cells may enlighten the pathogenesis of acute pancreatitis and help provide potential therapeutic targets for this disease.