IMR Press / FBS / Volume 16 / Issue 1 / DOI: 10.31083/j.fbs1601005
Open Access Review
Mitochondrial Dysfunction as a Factor of Energy Metabolism Disorders in Type 2 Diabetes Mellitus
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1 Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, 125315 Moscow, Russia
2 Sechenov First Moscow State Medical University (Sechenov University), 119991 Moscow, Russia
*Correspondence: (Alexander Blagov); (Alexander Orekhov)
Front. Biosci. (Schol Ed) 2024, 16(1), 5;
Submitted: 30 September 2023 | Revised: 15 December 2023 | Accepted: 4 January 2024 | Published: 8 March 2024
Copyright: © 2024 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

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.

type 2 diabetes
insulin resistance
mitochondrial dysfunction
#23-45-00031/Russian Science Foundation
Fig. 1.
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