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钙、线粒体与急性胰腺炎的发生。

Calcium, mitochondria and the initiation of acute pancreatitis.

机构信息

Division of Digestive and Liver Diseases, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.

Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, 90048, USA.

出版信息

Pancreatology. 2022 Nov;22(7):838-845. doi: 10.1016/j.pan.2022.07.011. Epub 2022 Aug 3.

DOI:10.1016/j.pan.2022.07.011
PMID:35941013
Abstract

Acute pancreatitis is characterized by necrosis of its parenchymal cells and influx and activation of inflammatory cells that further promote injury and necrosis. This review is intended to discuss the central role of disorders of calcium metabolism and mitochondrial dysfunction in the mechanism of pancreatitis development. The disorders are placed in context of calcium and mitochondria in physiologic function of the pancreas. Moreover, we discuss potential therapeutics for preventing pathologic calcium signals that injure mitochondria and interventions that promote the removal of injured mitochondria and regenerate new and heathy populations of mitochondria.

摘要

急性胰腺炎的特征是实质细胞坏死和炎症细胞的涌入和激活,进一步促进损伤和坏死。本文旨在讨论钙代谢紊乱和线粒体功能障碍在胰腺炎发病机制中的核心作用。这些紊乱是在胰腺的生理功能中钙和线粒体的背景下进行讨论的。此外,我们还讨论了预防病理性钙信号损伤线粒体的潜在治疗方法,以及促进清除受损线粒体和再生新的健康线粒体群体的干预措施。

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