Folliculogenesis, inheritance, and mitochondrial diseases: a review article

Oocyte mitochondria are unique organs that are established from the basal population in the primordial bud. Oocytes are formed in the mammalian ovary after birth, during folliculogenesis, and have a fundamental role in energy production and cellular processes, including metabolism and signal transduction. Each mitochondrion contains 5-10 copies of the mitochondrial genome, therefore each cell contains several hundreds to thousands of mitochondrial genomes. In most organisms, including humans, the father's mitochondria, which enter the ovule through the sperm, are never transmitted to the children, so the inheritance pattern of the mitochondrial genome has a maternal pattern.

Related articles from WILY ONLINE LIBRARY, ISI Web of Science, Link Springer, ScienceDirect, and Pubmed databases from 1963 to 2022 in which inheritance patterns, maternal inheritance, mitochondria, and mitochondrial diseases were searched and studied.

The findings indicate that the removal of paternal mitochondria and mechanisms related to ubiquinone, proteasome, and autophagy cause the destruction of paternal mitochondria and prevent the transfer of the mitochondrial genome. Mitochondrial diseases are mitochondrial changes in adult tissues and the resulting differences in clinical manifestations, so the mediating mechanisms in the relationship between genetic variation and human diseases are still a mystery, mainly due to problems in modeling.

Mitochondrial diseases caused by mutation of the mitochondrial genome in the maternal pattern caused by mutations in mitochondria are seen in MELAS, MERRF, NARP syndromes, Leigh, oligosymptomatic syndromes, diabetes mellitus, cardiomyopathy, myoglobinuria, and sensory-neural deafness. Therefore, the recognition of this mutation can be the target of gene therapy in the future.