Mitochondrial Dynamics and Insulin Secretion

被引:13
|
作者
Kabra, Uma D. [1 ]
Jastroch, Martin [2 ]
机构
[1] Parul Univ, Parul Inst Pharm, Dept Pharmaceut Chem, Vadodara 391760, India
[2] Stockholm Univ, Wenner Gren Inst, Dept Mol Biosci, Arrhenius Labs F3, SE-10691 Stockholm, Sweden
关键词
diabetes; mitochondrial dynamics; glucose-stimulated insulin secretion; pancreatic beta cell; fusion; fission; PANCREATIC BETA-CELLS; DOMINANT OPTIC ATROPHY; GLUCOSE-HOMEOSTASIS; DIABETES-MELLITUS; DRP1; RECRUITMENT; MITOFUSIN; FISSION; FUSION; GTPASE; OPA1;
D O I
10.3390/ijms241813782
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mitochondria are involved in the regulation of cellular energy metabolism, calcium homeostasis, and apoptosis. For mitochondrial quality control, dynamic processes, such as mitochondrial fission and fusion, are necessary to maintain shape and function. Disturbances of mitochondrial dynamics lead to dysfunctional mitochondria, which contribute to the development and progression of numerous diseases, including Type 2 Diabetes (T2D). Compelling evidence has been put forward that mitochondrial dynamics play a significant role in the metabolism-secretion coupling of pancreatic beta cells. The disruption of mitochondrial dynamics is linked to defects in energy production and increased apoptosis, ultimately impairing insulin secretion and beta cell death. This review provides an overview of molecular mechanisms controlling mitochondrial dynamics, their dysfunction in pancreatic beta cells, and pharmaceutical agents targeting mitochondrial dynamic proteins, such as mitochondrial division inhibitor-1 (mdivi-1), dynasore, P110, and 15-oxospiramilactone (S3).
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页数:19
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