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POSTER PRESENTATION / POSTER SUNUM



                                              Mitochondrial Pharmacotherapy

                          Gizem Erdoğan DURAN                        Begüm YURDAKÖK DIKMEN
                                                 1,*
                                                                                                  2

                ¹Ankara University, Graduate School of Health Sciences, Veterinary Pharmacology and Toxicology,
                                                      Ankara, TÜRKİYE
                 2 Ankara University, Faculty of Veterinary Medicine, Department of Pharmacology and Toxicology,
                                                      Ankara, TÜRKİYE

               *Correspound Author: gizemerdgnvet@gmail.com


                     Mitochondrial pharmacotherapy refers to therapeutic approaches aimed at correcting
               mitochondrial dysfunctions through the use of pharmacological agents targeting
               mitochondria.  Within  this  scope,  antioxidant  and  metabolic  support  agents  such  as
               coenzyme Q10, elamipretide, idebenone, and nicotinamide riboside are considered primary
               examples of conventional mitochondrial pharmacotherapy.

                     In recent years, however, cellular-based strategies that go beyond the boundaries of
               classical pharmacotherapy and aim to directly restore mitochondrial function have been
               developed. In this context, mitochondrial transplantation emerges as an innovative method,
               reflecting the evolving landscape of mitochondrial therapeutics.

                     Mitochondrial transplantation is based on the isolation of healthy mitochondria from
               one cell or tissue and their transfer into target cells or tissues  exhibiting mitochondrial
               dysfunction. This approach is employed to support cellular energy production and to restore
               mitochondrial function. The intercellular  transfer of mitochondria occurs through
               mechanisms such as tunneling nanotubes (TNT), extracellular vesicles, dendritic networks,
               and cell fusion.

                     Transplantation has been reported to yield promising outcomes  in disease models
               involving organs such as the liver, brain, heart, kidney, and lung. Following the procedure,
               biological effects such as increased ATP levels, reduction of oxidative stress and
               inflammatory responses, suppression of apoptosis, and reintegration of the mitochondrial
               network via fusion  have been observed. These improvements are  reflected clinically  in
               reduced ischemic lesion sizes, recovery of organ functions (cardiac, neurological, pulmonary,
               and renal parameters), and decreased histopathological damage.

                     This review will address the pharmacotherapeutic applications, clinical potential, and
               possible adverse effects of mitochondrial transplantation. The limited number of studies in
               the field of veterinary medicine and the lack of standardized, optimized protocols for current
               applications make this topic particularly significant in the literature.

               Keywords: Mitochondrial Pharmacotherapy, Mitochondrial Transplantation, Oxidative Stress,
               ATP.




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