Literature Review Open Access

Mitochondrial Dysfunction Model in the Pathogenesis of Inflammatory Response Development in Obesity

Alexander Blagov1, Varvara Orekhova1,2, Vasily Sukhorukov1,2, Alexandra Melnichenko1 and Alexander Orekhov1,2
  • 1 Department of General Pathology, Laboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, Russia
  • 2 Institute for Atherosclerosis Research, Moscow, Russia

Abstract

Obesity is one of the growing problems of modern society. Although currently used methods of treating obesity, including diet, exercise, and drug therapy, have shown their applicability to more effectively combat obesity, an understanding of the pathogenesis of this disease is required. One of the insufficiently studied factors in the pathogenesis of obesity is the development of mitochondrial dysfunction understanding the role of which in the development of obesity will make it possible to find new ways to combat this disease. The review was created by analyzing evidence from the most promising studies on the pathogenesis of obesity. The main aim of this review was to develop a model of the pathogenesis of obesity, the central link in which is the development of mitochondrial dysfunction. An additional aim was to propose, based on the developed model, a number of potential therapeutic strategies for the treatment of obesity. Increased nutrient intake leads to the disruption of the electron transport chain work, which causes an increase in the production of reactive oxygen species, which causes: (1) Damage to mitochondria and as a result, mitochondrial dysfunction, impaired energy metabolism, and increasing oxidative stress, (2) As well as damage to other cellular structures and as a result, the accumulation of toxic oxidation products and immunogenic molecules. Together, this leads to chronic inflammation and the development of insulin resistance, which is the high-risk factor for diabetes. Compounds aimed at normalizing the function of mitochondria, such as L-carnitine and ubiquinone, can be proposed as additional therapies. Aerobic exercise also contributes to the normalization of mitochondrial function.

OnLine Journal of Biological Sciences
Volume 24 No. 1, 2024, 110-120

DOI: https://doi.org/10.3844/ojbsci.2024.110.120

Submitted On: 29 June 2023 Published On: 19 November 2023

How to Cite: Blagov, A., Orekhova, V., Sukhorukov, V., Melnichenko, A. & Orekhov, A. (2024). Mitochondrial Dysfunction Model in the Pathogenesis of Inflammatory Response Development in Obesity. OnLine Journal of Biological Sciences, 24(1), 110-120. https://doi.org/10.3844/ojbsci.2024.110.120

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Keywords

  • Mitochondrial Dysfunction
  • Mitochondria
  • Pathogenesis
  • Obesity
  • Reactive Oxygen Species