The role of mitochondria in premature ovarian failure: A review
DOI:
https://doi.org/10.22317/jcms.v6i1.712Keywords:
Premature ovarian failure, Mitochondria, Infertility, low ovarian reserveAbstract
Premature ovarian failure (POF) is used to describe women under 40 years old with amenorrhea, hypergonadotropic hypogonadism, and infertility as a result of cessation of ovarian function. It has been reported that almost 20% of women who consult for infertility have signs of premature ovarian ageing. The mitochondrial disorder is one of the critical agents in premature menopause and the occurrence of POF. Due to the maternal inheritance of POF along with the dependence of folliculogenesis upon the mitochondrial biogenesis and bioenergetics, it has been suggested that a generalized mitochondrial defect is likely involved in POF. A fuller understanding of the mitochondrial role in POF could contribute to the better management of women with POF in the future. The aim of this review was to illustrate the role of mitochondria in POF. The oocyte mitochondrial DNA (mtDNA) content in women with diminished ovarian reserve is significantly lower than in women with normal ovarian reserve. It has been evidenced that mitochondrial genetic disorders and mitochondrial oxidative stress are associated with POF. According to the maternal inheritance of mtDNA, genetic testing should be performed to detect mtDNA mutations involved in POF before starting treatment strategies. If these mutations are present, it could suggest that healthy mitochondrial transfer during ART should be used to prevent the transmission of POF caused by mtDNA mutation to the female offspring. Future strategies aimed at treatment of POF-related infertility should take into account the significance of the oocyte mitochondrial role in the occurrence of this disorder.
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39. Kaguni LS. DNA polymerase γ, the mitochondrial replicase. Annual review of biochemistry. 2004;73(1):293-320.
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41. Van Goethem G, Dermaut B, Löfgren A, Martin J-J, Van Broeckhoven C. Mutation of POLG is associated with progressive external ophthalmoplegia characterized by mtDNA deletions. Nature genetics. 2001;28(3):211.
42. Stumpf JD, Saneto RP, Copeland WC. Clinical and molecular features of POLG-related mitochondrial disease. Cold Spring Harbor perspectives in biology. 2013;5(4):a011395.
43. Tong Z-B, Sullivan SD, Lawless LM, Vanderhoof V, Zachman K, Nelson LM. Five mutations of mitochondrial DNA polymerase-gamma (POLG) are not a prevalent etiology for spontaneous 46, XX primary ovarian insufficiency. Fertility and sterility. 2010;94(7):2932-4.
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50. Prasad S, Tiwari M, Pandey AN, Shrivastav TG, Chaube SK. Impact of stress on oocyte quality and reproductive outcome. Journal of biomedical science. 2016;23(1):36.
51. Khodamoradi K, Amini-Khoei H, Khosravizadeh Z, Hosseini SR, Dehpour AR, Hassanzadeh G. Oxidative stress, inflammatory reactions and apoptosis mediated the negative effect of chronic stress induced by maternal separation on the reproductive system in male mice. Reproductive biology. 2019;19(4):340-8.
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Published
2020-02-26
How to Cite
Khosravizadeh, Z., Rashidi, Z., Talebi, A., Khodamoradi, K., & Hassanzadeh, G. (2020). The role of mitochondria in premature ovarian failure: A review. Journal of Contemporary Medical Sciences, 6(1), 1–7. https://doi.org/10.22317/jcms.v6i1.712
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Review
