Interplay between maternal nutrition and epigenetic programming on offspring hypertension

Tain, You-Lin; Hsu, Chien-Ning

doi:10.1016/j.jnutbio.2024.109604

Cited by 1 publication

(2 citation statements)

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“…AHR is a pivotal player in orchestrating epigenetic regulations impacting transcriptome alterations, chromatin architecture adjustments, and involvement in crucial signaling pathways [171]. Epigenetic mechanisms such as aberrant DNA methylation, histone modification, and microRNAs can drive changes in gene expression, potentially leading to developmental programming [172]. Chemical exposure-related developmental programming implicates various molecular pathways including oxidative stress, dysregulated nutrient-sensing signals, aberrant RAS, reduced nephron numbers, and dysbiotic gut microbiota, all intertwined with epigenetic programming [172][173][174][175][176][177].…”

Section: Othersmentioning

confidence: 99%

“…Epigenetic mechanisms such as aberrant DNA methylation, histone modification, and microRNAs can drive changes in gene expression, potentially leading to developmental programming [172]. Chemical exposure-related developmental programming implicates various molecular pathways including oxidative stress, dysregulated nutrient-sensing signals, aberrant RAS, reduced nephron numbers, and dysbiotic gut microbiota, all intertwined with epigenetic programming [172][173][174][175][176][177]. Given the interconnectedness of these mechanisms with AHR signaling, there exists significant potential for cross-talk among them in the context of CKM programming.…”

Section: Othersmentioning

confidence: 99%

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The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular–Kidney–Metabolic Programming

Tain,

Hsu

2024

IJMS

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Early life exposure lays the groundwork for the risk of developing cardiovascular–kidney–metabolic (CKM) syndrome in adulthood. Various environmental chemicals to which pregnant mothers are commonly exposed can disrupt fetal programming, leading to a wide range of CKM phenotypes. The aryl hydrocarbon receptor (AHR) has a key role as a ligand-activated transcription factor in sensing these environmental chemicals. Activating AHR through exposure to environmental chemicals has been documented for its adverse impacts on cardiovascular diseases, hypertension, diabetes, obesity, kidney disease, and non-alcoholic fatty liver disease, as evidenced by both epidemiological and animal studies. In this review, we compile current human evidence and findings from animal models that support the connection between antenatal chemical exposures and CKM programming, focusing particularly on AHR signaling. Additionally, we explore potential AHR modulators aimed at preventing CKM syndrome. As the pioneering review to present evidence advocating for the avoidance of toxic chemical exposure during pregnancy and deepening our understanding of AHR signaling, this has the potential to mitigate the global burden of CKM syndrome in the future.

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