Open AccessThe role of mitochondria in premature ovarian failure: A review
Author(s) -
Zahra Khosravizadeh,
Zahra Rashidi,
Ali Talebi,
Kajal Khodamoradi,
Gholamreza Hassanzadeh
Publication year - 2020
Publication title -
journal of contemporary medical sciences
Language(s) - English
Resource type - Journals
eISSN - 2415-1629
pISSN - 2413-0516
DOI - 10.22317/jcms.v6i1.712
Subject(s) - mitochondrial dna , premature ovarian failure , biology , infertility , mitochondrial biogenesis , mitochondrion , ovarian reserve , non mendelian inheritance , genetics , oocyte , physiology , andrology , endocrinology , medicine , pregnancy , gene , embryo
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.