Autologous mitochondrial microinjection; A strategy to improve the oocyte quality and subsequent reproductive outcome during aging

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Abstract

Along with the decline in oocyte quality, numerous defects such as mitochondrial insufficiency and the increase of mutation and deletion have been reported in oocyte mitochondrial DNA (mtDNA) following aging. Any impairments in oocyte mitochondrial function have negative effects on the reproduction and pregnancy outcome. It has been stated that infertility problems caused by poor quality oocytes in women with in vitro fertilization (IVF) and repeated pregnancy failures are associated with aging and could be overcome by transferring large amounts of healthy mitochondria. Hence, researches on biology, disease, and the therapeutic use of mitochondria continue to introduce some clinical approaches such as autologous mitochondrial transfer techniques. Following mitochondrial transfer, the amount of ATP required for aged-oocyte during fertilization, blastocyst formation, and subsequent embryonic development could be an alternative modality. These modulations improve the pregnancy outcome in women of high reproductive aging as well. In addition to overview the clinical studies using mitochondrial microinjection, this study provides a framework for future approaches to develop effective treatments and preventions of congenital transmission of mitochondrial DNA mutations/diseases to offspring. Mitochondrial transfer from ovarian cells and healthy oocytes could lead to improved fertility outcome in low-quality oocytes. The modulation of mitochondrial bioactivity seems to regulate basal metabolism inside target oocytes and thereby potentiate physiological activity of these cells while overcoming age-related infertility in female germ cells.

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Mobarak, H., Heidarpour, M., Tsai, P. S. J., Rezabakhsh, A., Rahbarghazi, R., Nouri, M., & Mahdipour, M. (2019, November 29). Autologous mitochondrial microinjection; A strategy to improve the oocyte quality and subsequent reproductive outcome during aging. Cell and Bioscience. BioMed Central Ltd. https://doi.org/10.1186/s13578-019-0360-5

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