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.
A wide variety of cell populations, including both immune and endothelial cells, participate in the pathogenesis of atherosclerosis. Among these groups, macrophages deserve special attention because different populations of them can have completely different effects on atherogenesis and inflammation in atherosclerosis. In the current review, the significance of different phenotypes of macrophages in the progression or regression of atherosclerosis will be considered, including their ability to become the foam cells and the consequences of this event, as well as their ability to create a pro-inflammatory or anti-inflammatory medium at the site of atherosclerotic lesions as a result of cytokine production. In addition, several therapeutic strategies directed to the modulation of macrophage activity, which can serve as useful ideas for future drug developments, will be considered.
The prevalence of multiple sclerosis and the complexity of its etiology and pathogenesis require further study of the factors underlying the progression of this disease. The prominent role of mitochondria in neurons makes this organelle a vulnerable target for CNS diseases. The purpose of this review is to consider the role of mitochondrial dysfunction in the pathogenesis of multiple sclerosis, as well as to propose new promising therapeutic strategies aimed at restoring mitochondrial function in multiple sclerosis.
Impaired mitophagy is one of the hallmarks of the pathogenesis of Parkinson’s disease, which highlights the importance of the proper functioning of mitochondria, as well as the processes of mitochondrial dynamics for the functioning of dopaminergic neurons. At the same time, the main factors leading to disruption of mitophagy in Parkinson’s disease are mutations in the Pink1 and Parkin enzymes. Based on the characterized mutant forms, the marked cellular localization, and the level of expression in neurons, these proteins can be considered promising targets for the development of drugs for Parkinson’s therapy. This review will consider such class of drug compounds as mitophagy activators and these drugs in the treatment of Parkinson’s disease.
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.
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