A perinatal approach for unraveling mitochondrial function in preeclampsia and fetal growth restriction: a role for...

Area of Science:

• Obstetrics and Gynecology
• Cardiovascular Medicine
• Mitochondrial Biology

Background:

• Preeclampsia (PE) and fetal growth restriction (FGR) are placental insufficiency syndromes.
• These conditions significantly contribute to maternal and fetal morbidity and mortality.
• Mitochondrial dysfunction is implicated in the pathophysiology of PE and FGR, leading to organ damage and later cardiovascular disease risk.

Purpose of the Study:

• To review the effects of PE and FGR on mitochondrial function across maternal and fetal organs.
• To explore the underlying mechanisms of mitochondrial dysfunction in these conditions.
• To investigate the potential of mitochondrial targeted therapies for PE and FGR.

Main Methods:

• Systematic review of literature focusing on placental insufficiency syndromes.
• Perinatal approach examining maternal and fetal heart and kidney, and placenta.
• Analysis of mitochondrial function, oxidative stress, metabolic pathways, quality control, and calcium handling.

Main Results:

• Placental insufficiency syndromes like PE and FGR critically impair mitochondrial function.
• Mitochondrial dysfunction affects maternal and fetal organ systems, including the heart and kidneys.
• Evidence suggests a link between these conditions and increased risk of future cardiovascular disease.

Conclusions:

• Mitochondrial function is central to the pathophysiology of PE and FGR.
• Targeting mitochondrial pathways (oxidative stress, metabolism, quality control, calcium handling) holds therapeutic potential.
• Further research and targeted therapies are needed to improve maternal and fetal outcomes and long-term cardiovascular health.