1. Oxidative Stress and Mitochondrial Health in Male Reproductive Health.

 Male infertility is a growing problem that affects 30% of infertile human couples due to a decline in sperm counts and a rise in testicular and sperm anomalies. The evaluation of male factor infertility has become more important and informative since new diagnostic techniques and therapeutic options have become available. The respiratory dysfunction of mitochondria probably causes a decline in motility. We suggested that redox control in the mitochondrial microenvironment is essential for proper sperm motility and fertility.

2. Estrogen Receptor contributes to Human Disease.  

Estrogen is the major regulator of cellular growth, energy production, biogenesis, and apoptosis. Estrogen enhances mitochondrial function by enhancing mitochondrial biogenesis and sustaining mitochondrial energy–transducing capacity. Studies have shown that mitochondria are an important target of estrogen. Estrogen receptor-beta (ERβ) has been shown to localize to mitochondria in a ligand-dependent or --independent manner and can affect mitochondrial bioenergetics and anti-apoptotic signaling. 

3. Mitochondrial Health in Female Reproduction. 

Mitochondria are vital organelles involved in cellular energy production and programmed cell death. Concurrently, mitochondria are the central sites for steroid hormone biosynthesis. The first and rate-limiting step in the biosynthesis of steroid hormones occurs in the mitochondria of granulosa cells. In the present study, we hypothesized that the mitochondria in granulosa cells are critical for maintaining oocyte quality and fertility capacity. We found mitochondrial dysfunction of human granulosa cells may contribute to the decline of steroidogenesis, decreased fertilization rate, oocyte maturation rate, and oocyte quality, and it can ultimately jeopardize fertility. 

4.  Mitochondrial Health in Human Diseases 

As the center organelle of the intrinsic apoptotic pathways, mitochondria are the reservoir of proapoptotic factors. Impairing mitochondrial function causes cell death by compromising ATP production, calcium homeostasis and increasing oxidative stress. Therefore, mitochondrial dysfunction is rationally suspected to be a causal link to human diseases. In addition, mitochondrial dysfunction occurs when the mitochondria don't work as well as they should due to another disease or condition. Many conditions can lead to secondary mitochondrial dysfunction and affect several human diseases. Recently, we tried to understand the role of mitochondria in metabolic disease and mitochondrial diseases.