The role of mitochondria as a regulator in the intracellular physiological pathways is a field that has recently been incorporated into the reproduction area. Thus, the mechanisms that explain mitochondrial dysfunction and its impact on reproduction become an area of great importance to study. Mitochondrial ...
The role of mitochondria as a regulator in the intracellular physiological pathways is a field that has recently been incorporated into the reproduction area. Thus, the mechanisms that explain mitochondrial dysfunction and its impact on reproduction become an area of great importance to study. Mitochondrial diseases and mitochondrial aging impact fertility. There are technologies focused on oocyte mitochondrial DNA copy. Although maternal mitochondrial inheritance is crucial in the fate of the embryo, it has not been described oocyte mitochondrial marker yet, as a good factor to predict its quality. In addition, little is known about the role of mitochondria-derived peptides (MDPs) in reproduction. Humanin is one of the MDP codified in the open reading frame in mitochondrial DNA. It was described that HN is a cytoprotective factor against different stressors in the testicle and ovary. Even, it was associated with ovarian and testicular aging protection.
This collection aims to highlight the importance of mitochondria in reproduction. Topic Editors welcome manuscripts focused on, but not limited to, the following themes:
- New mitochondrial pathways linking to follicular development and ovarian aging;
- Mitochondria as a therapeutic target for reproductive diseases;
- MDPs as anti-oxidant factors in reproduction;
- MDPs in ovarian or testicle cancer.
Keywords:
humanin, reproduction, aging, ovaries, cancer
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.