MRC Group, School of Biosciences, Biomedical Sciences Building, Museum Avenue, Cardiff, CF10 3AX, Wales, UK.
Pflugers Arch. 2012 Jul;464(1):89-99. doi: 10.1007/s00424-012-1117-8. Epub 2012 Jun 1.
As a primary energy producer, mitochondria play a fundamental role in pancreatic exocrine physiology and pathology. The most frequent aetiology of acute pancreatitis is either gallstones or heavy alcohol consumption. Repeated episodes of acute pancreatitis can result in the development of chronic pancreatitis and increase the lifetime risk of pancreatic cancer 100-fold. Pancreatic cancer is one of the most common causes of cancer mortality with only about 3-4 % of patients surviving beyond 5 years. It has been shown that acute pancreatitis involves Ca²⁺ overload and overproduction of reactive oxygen species in pancreatic acinar cells. Both factors significantly affect mitochondria and lead to cell death. The pathogenesis of inflammation in acute and chronic pancreatitis is tightly linked to the induction of necrosis and apoptosis. There is currently no specific therapy for pancreatitis, but recent findings of an endogenous protective mechanism against Ca²⁺ overload--and particularly the potential to boost this protection--bring hope of new therapeutic approaches.
作为主要的能量产生者，线粒体在胰腺外分泌生理学和病理学中起着至关重要的作用。急性胰腺炎最常见的病因是胆石症或大量饮酒。反复发作的急性胰腺炎可导致慢性胰腺炎的发展，并使胰腺癌的终身风险增加 100 倍。胰腺癌是癌症死亡的最常见原因之一，只有约 3-4%的患者能存活超过 5 年。已经表明，急性胰腺炎涉及胰腺腺泡细胞中的 Ca²⁺超载和活性氧的过度产生。这两个因素都显著影响线粒体并导致细胞死亡。急性和慢性胰腺炎的炎症发病机制与坏死和细胞凋亡的诱导密切相关。目前尚无针对胰腺炎的特异性治疗方法，但最近发现了一种针对 Ca²⁺超载的内源性保护机制——特别是增强这种保护的潜力——为新的治疗方法带来了希望。
