Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia.
Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia.
Front Biosci (Schol Ed). 2024 Mar 8;16(1):5. doi: 10.31083/j.fbs1601005.
The pathogenesis of type 2 diabetes mellitus (T2DM) is based on the development of insulin resistance, which is a disruption to the ability of the tissues to bind to insulin, leading to a general metabolic disorder. Mitochondria are the main participants in cellular energy metabolism, meaning their dysfunction is associated with the development of insulin resistance in T2DM. Mitochondrial function is affected by insulin resistance in various tissues, including skeletal muscle and the liver, which greatly influence glucose homeostasis throughout the body. This review studies mitochondrial dysfunction in T2DM and its impact on disease progression. In addition, it considers the causes underlying the development of mitochondrial dysfunction in T2DM, including mutations in the mitochondrial genome, mitochondrial DNA methylation, and other epigenetic influences, as well as the impact of impaired mitochondrial membrane potential. New therapeutic strategies for diabetes that have been developed to target the mitochondria will also be presented.
2 型糖尿病（T2DM）的发病机制基于胰岛素抵抗的发展，这是组织与胰岛素结合能力的破坏，导致一般代谢紊乱。线粒体是细胞能量代谢的主要参与者，这意味着它们的功能障碍与 T2DM 中胰岛素抵抗的发展有关。胰岛素抵抗会影响包括骨骼肌和肝脏在内的各种组织中的线粒体功能，这极大地影响了全身的葡萄糖稳态。本综述研究了 T2DM 中的线粒体功能障碍及其对疾病进展的影响。此外，还考虑了导致 T2DM 中线粒体功能障碍的原因，包括线粒体基因组突变、线粒体 DNA 甲基化和其他表观遗传影响，以及受损的线粒体膜电位的影响。还将介绍针对线粒体开发的新的糖尿病治疗策略。
