Mitochondrial dysfunction and oxidative stress in selective fetal growth restriction
Yucheng Hu1, Yuhong Lin1, Jiawen Yang1
1The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, China; Shanghai Key Laboratory of Embryo Original Diseases, Shanghai, 200030, China.
Placenta
|September 12, 2024
Summary
Mitochondrial dysfunction and oxidative stress in placental tissue contribute to selective fetal growth restriction (sFGR). Genetic and epigenetic changes in mitochondria may underlie these placental defects, impacting fetal development.
Area of Science:
- Perinatology
- Mitochondrial Biology
- Genetics
Background:
- Placental dysfunction is a key factor in selective fetal growth restriction (sFGR).
- The precise role of mitochondria in sFGR pathogenesis is not fully understood.
Purpose of the Study:
- To investigate mitochondrial functional defects in sFGR placentas.
- To explore the contribution of mitochondrial genomic and epigenetic alterations to sFGR.
Main Methods:
- Analysis of placental villi from monochorionic diamniotic (MCDA) twins with sFGR.
- Assessment of mitochondrial morphology, reactive oxygen species (ROS), ATP levels, and oxidative damage markers.
- Mitochondrial DNA (mtDNA) copy number analysis, sequencing, and methylation sequencing.
- Evaluation of specific gene and lncRNA expression.
Main Results:
- sFGR placentas exhibit significant mitochondrial damage in cytotrophoblasts and increased mitochondrial numbers in syncytiotrophoblasts.
- Elevated oxidative stress, increased ROS production, and reduced ATP generation were observed in sFGR placentas.
- Increased mtDNA copy number, a mutation in MT-RNR2, altered expression of COX I and specific lncRNAs were identified in sFGR placentas.
Conclusions:
- Oxidative stress and mitochondrial dysfunction are exacerbated in sFGR placentas.
- Compromised energy production and failed compensatory mechanisms may stem from mitochondrial genetic mutations and aberrant epigenetic regulation.
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