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Mitochondria play a central role in energy metabolism and cell survival. They often undergo structural and dynamic changes under various types of stress and impaired energy homeostasis. In addition to the intracellular movement of mitochondria, their intercellular transport is of great importance. Intercellular transfer occurs in both physiological conditions and various pathologies. It is accompanied by elimination of damage in stressed cells and the restoration of structural and functional tissue disorders caused by mitochondrial dysfunction. This review summarizes the latest data accumulated in this area and provides a general idea on the molecular mechanisms of mitochondrial intercellular transport and its role in maintaining energy homeostasis in tissues. Promising ways of studying mitochondrial transfer for targeted therapy of many diseases are discussed separately. [ABSTRACT FROM AUTHOR]

Tunneling nanotubes (TNTs) are thin membrane elongations among the cells that mediate the trafficking of subcellular organelles, biomolecules, and cues. Mesenchymal stem cells (MSCs) receive substantial attention in tissue engineering and regenerative medicine. Many MSCs-based clinical trials are ongoing for dreadful diseases including cancer and neurodegenerative diseases. Mitochondrial trafficking through TNTs is one of the mechanisms used by MSCs to repair tissue damage and to promote tissue regeneration. Preclinical studies linked with ischemia, oxidative stress, mitochondrial damage, inflammation, and respiratory illness have demonstrated the therapeutic efficacy of MSCs via TNTs-mediated transfer of mitochondria and other molecules into the injured cells. On the other hand, MSCs-based cancer studies showed that TNTs may modulate chemoresistance in tumor cells as a result of mitochondrial trafficking. In the present review, we discuss the role of TNTs from preclinical studies associated with MSCs treatment. We discuss the impact of TNTs formation between MSCs and cancer cells and emphasize to study the importance of TNTs-mediated MSCs protection in disease models. [ABSTRACT FROM AUTHOR]