Atherosclerosis · 2026
Differential methylation of lipid metabolism and X-linked inheritance genes is associated with low placental efficiency, impaired fatty acid metabolism and oxidative stress in the placenta of hypercholesterolemic mothers.
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Jayalekshmi V S, Basu Budhaditya, Srijith Sreelekshmi, Krishna Geethu, Rafeekha P, Vidyalekshmy R, Ramachandran Surya
Аннотация
BACKGROUND: Maternal hypercholesterolemia (MHC), characterized by elevated cholesterol levels in mothers during gestation, increases the risk of atherosclerosis in offspring. This study seeks to uncover how in-utero fetal programming may be linked to changes in methylation patterns in the placenta, potentially affecting fetal gene expression.
METHODS: Pregnant subjects who were within the first 100 days of gestation were recruited and classified as either normocholesterolemic (NC) or hypercholesterolemic (MHC). Lipid profiling was conducted throughout all trimesters. Post delivery, placental samples were collected, and newborn parameters were recorded. A genome-wide methylation EPIC array and histological analysis were performed on the placental samples, with results validated using quantitative real-time PCR and immunohistochemistry.
RESULTS: EPIC array analysis revealed significant methylation changes in genes linked to X-linked inheritance and lipid metabolism pathways. Combined gene expression studies and histopathological analysis indicated disrupted fatty acid metabolism and elevated oxidative stress in placentas affected by maternal hypercholesterolemia (MHC). Furthermore, MHC was associated with decreased placental efficiency, lower birth weight, elongated umbilical cords in newborns.
CONCLUSIONS: Maternal hypercholesterolemia is associated with methylation changes in the placenta that disrupt metabolic pathways and compromise placental function. This study offers strong experimental evidence that the MHC placenta plays a role in fetal programming, contributing to clinical manifestations in offspring.
METHODS: Pregnant subjects who were within the first 100 days of gestation were recruited and classified as either normocholesterolemic (NC) or hypercholesterolemic (MHC). Lipid profiling was conducted throughout all trimesters. Post delivery, placental samples were collected, and newborn parameters were recorded. A genome-wide methylation EPIC array and histological analysis were performed on the placental samples, with results validated using quantitative real-time PCR and immunohistochemistry.
RESULTS: EPIC array analysis revealed significant methylation changes in genes linked to X-linked inheritance and lipid metabolism pathways. Combined gene expression studies and histopathological analysis indicated disrupted fatty acid metabolism and elevated oxidative stress in placentas affected by maternal hypercholesterolemia (MHC). Furthermore, MHC was associated with decreased placental efficiency, lower birth weight, elongated umbilical cords in newborns.
CONCLUSIONS: Maternal hypercholesterolemia is associated with methylation changes in the placenta that disrupt metabolic pathways and compromise placental function. This study offers strong experimental evidence that the MHC placenta plays a role in fetal programming, contributing to clinical manifestations in offspring.