Mitochondrial dysfunction is now recognized as a contributing factor to neurodegenerative diseases, including Alzheimer’s disease (AD). Mitochondria are signaling organelles with a variety of functions ranging from energy production to the regulation of cellular metabolism, energy homeostasis, and response to stress. The successful functioning of these complex processes is critically dependent on the accuracy of mitochondrial dynamics, which includes the ability of mitochondria to change shape and position in the cell, which is necessary to maintain proper function and quality control, especially in polarized cells such as neurons. There has been much evidence to suggest that the disruption of mitochondrial dynamics may play a critical role in the pathogenesis of AD. This review highlights aspects of altered mitochondrial dynamics in AD that may contribute to the etiology of this debilitating condition. We also discuss therapeutic strategies to improve mitochondrial dynamics and function that may provide an alternative treatment approach.

Rheumatoid arthritis (RA) is a progressive autoimmune disease that affects the joints. It has been proven that, with the development of RA, there are changes in the metabolism of cells located in the focus of inflammation. In this article, we describe the connection between metabolism and inflammation in the context of rheumatoid arthritis. We consider in detail the changes in metabolic processes and their subsequent immunomodulatory effects. In particular, we consider how changes in mitochondrial functioning lead to the modulation of metabolism in rheumatoid arthritis. We also describe the main features of the metabolism in cells present in the synovial membrane during inflammation, and we discuss possible targets for the therapy of rheumatoid arthritis.

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.

Crohn’s disease remains one of the challenging problems of modern medicine, and the development of new and effective and safer treatments against it is a dynamic field of research. To make such developments possible, it is important to understand the pathologic processes underlying the onset and progression of Crohn’s disease at the molecular and cellular levels. During the recent years, the involvement of mitochondrial dysfunction and associated chronic inflammation in these processes became evident. In this review, we discuss the published works on pathogenetic models of Crohn’s disease. These models make studying the role of mitochondrial dysfunction in the disease pathogenesis possible and advances the development of novel therapies.