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Trends Mol Med. 2015 Feb;21(2):68-76. doi: 10.1016/j.molmed.2014.12.001. Epub 2014 Dec 10.

Mitochondrial replacement therapy in reproductive medicine.

Author information

1
Center for Embryonic Cell and Gene Therapy, Oregon Health & Science University, 3303 S.W. Bond Avenue, Portland, OR 97239, USA; Division of Reproductive & Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, 505 N.W. 185th Avenue, Beaverton, OR 97006, USA.
2
Center for Embryonic Cell and Gene Therapy, Oregon Health & Science University, 3303 S.W. Bond Avenue, Portland, OR 97239, USA; Division of Reproductive & Developmental Sciences, Oregon National Primate Research Center, Oregon Health & Science University, 505 N.W. 185th Avenue, Beaverton, OR 97006, USA. Electronic address: mitalipo@ohsu.edu.

Abstract

Mitochondrial dysfunction is implicated in disease and age-related infertility. Mitochondrial replacement therapies (MRT) in oocytes or zygotes, such as pronuclear (PNT), spindle (ST), or polar body (PBT) transfer, could prevent second-generation transmission of mitochondrial DNA (mtDNA) defects. PNT, associated with high levels of mtDNA carryover in mice but low levels in human embryos, carries ethical issues secondary to donor embryo destruction. ST, developed in primates, supports normal development to adults and low mtDNA carryover. PBT in mice, coupled with PN or ST, may increase the yield of reconstructed embryos with low mtDNA carryover. MRT also offers replacement of the deficient cytoplasm in oocytes from older patients, with the expectation of high pregnancy rates following in vitro fertilization.

KEYWORDS:

female infertility; mitochondria; mitochondrial DNA; mitochondrial replacement therapy

PMID:
25573721
PMCID:
PMC4377089
DOI:
10.1016/j.molmed.2014.12.001
[Indexed for MEDLINE]
Free PMC Article

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