Abstract
Mitochondria are well known as ‘the powerhouses of the cell’. Indeed, their major role is cellular energy production driven by both mitochondrial and nuclear DNA. Such a feature makes these organelles essential for successful fertilisation and proper embryo implantation and development. Generally, mitochondrial DNA is exclusively maternally inherited; oocyte’s mitochondrial DNA level is crucial to provide sufficient ATP content for the developing embryo until the blastocyst stage of development. Additionally, human fertility and early embryogenesis may be affected by either point mutations or deletions in mitochondrial DNA. It was suggested that their accumulation may be associated with ovarian ageing. If so, is mitochondrial dysfunction the cause or consequence of ovarian ageing? Moreover, such an obvious relationship of mitochondria and mitochondrial genome with human fertility and early embryo development gives the field of mitochondrial research a great potential to be of use in clinical application. However, even now, the area of assessing and improving DNA quantity and function in reproductive medicine drives many questions and uncertainties. This review summarises the role of mitochondria and mitochondrial DNA in human reproduction and gives an insight into the utility of their clinical use.
Highlights
Mitochondria are well known as ‘the powerhouses of the cell’; in recent years, our understanding of its biology has vastly increased
This review summarises the role of mitochondria and mitochondrial DNA (mtDNA) in human oocytes and embryos, showing its influence on fertility and early embryo development
The fission process is mediated by the dynamin-related protein 1 (DRP1) recruited from the cytosol to the outer mitochondrial membrane
Summary
Mitochondria are well known as ‘the powerhouses of the cell’; in recent years, our understanding of its biology has vastly increased. Mitochondria have their own genome which is replicated independently of the nuclear genome. The major role of mitochondria is to produce the ATP required by cells. This process relies on OXPHOS whose by-product is the generation of reactive oxygen species (ROS). Mitochondria can sequester and release Ca2+ regulating calcium responses [4,5]. They mediate cell proliferation, differentiation, and apoptosis [3–6]. We make an insight into the clinical usefulness of assessing and improving mtDNA quantity and function
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