This review deals with the roles of calcium and ATP in the control of the normal functions of the different cell types in the exocrine pancreas as well as the roles of these molecules in the pathophysiology of Acute Pancreatitis. Repetitive rises in the local cytosolic calcium ion concentration in the apical part of the acinar cells do not only activate exocytosis but also, via an increase in the intra-mitochondrial calcium ion concentration, stimulate the ATP formation that is needed to fuel the energy-requiring secretion process. However, intracellular calcium overload, resulting in a global sustained elevation of the cytosolic calcium ion concentration, has the opposite effect of decreasing mitochondrial ATP production and this initiates processes that lead to the necrotic destruction of the cells. In the last few years it has become possible to image calcium signalling events simultaneously in acinar, stellate and immune cells in intact lobules of the exocrine pancreas. This has disclosed processes by which these cells interact with each other, particularly in relation to the initiation and development of Acute Pancreatitis. By unravelling the molecular mechanisms underlying this disease, several promising therapeutic intervention sites have been identified. This provides hope that we may soon be able to effectively treat this often fatal disease.

中文翻译：

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钙和 ATP 在胰腺外分泌生理和病理学中的作用

这篇综述讨论了钙和 ATP 在控制胰腺外分泌不同细胞类型的正常功能中的作用，以及这些分子在急性胰腺炎病理生理学中的作用。腺泡细胞顶端局部细胞溶质钙离子浓度的反复升高不仅激活胞吐作用，而且通过增加线粒体内钙离子浓度，刺激 ATP 形成，这是为所需能量提供燃料所需的分泌过程。然而，细胞内钙超载，导致细胞溶质钙离子浓度的整体持续升高，具有降低线粒体 ATP 产生的相反作用，这会引发导致细胞坏死破坏的过程。在过去的几年里，在胰腺外分泌的完整小叶中同时对腺泡、星状和免疫细胞中的钙信号事件进行成像已经成为可能。这揭示了这些细胞相互作用的过程，特别是与急性胰腺炎的发生和发展有关的过程。通过揭示这种疾病的分子机制，已经确定了几个有希望的治疗干预位点。这为我们很快能够有效治疗这种通常致命的疾病提供了希望。通过揭示这种疾病的分子机制，已经确定了几个有希望的治疗干预位点。这为我们很快能够有效治疗这种通常致命的疾病提供了希望。通过揭示这种疾病的分子机制，已经确定了几个有希望的治疗干预位点。这为我们很快能够有效治疗这种通常致命的疾病提供了希望。