
Advanced Science, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 10, 2025
Abstract Bisphenol A (BPA) is an “environmental obesogen” and this study aims to investigate the intergenerational impacts of BPA‐induced metabolic syndrome (MetS), specifically focusing on unraveling mechanisms. Exposure BPA induces disorders in paternal mice, which are then transmitted offspring, leading late‐onset MetS. Mechanistically, upregulates Srebf1, turn promotes Pparg‐dependent transcription Dicer1 spermatocytes, increasing levels multiple sperm microRNAs (miRNAs). Several these miRNAs highly expressed a synchronized manner liver offspring. miR149‐5p, miR150‐5p, miR700‐5p target specific region Lepr 3′UTR, termed “SMITE” (“ S everal Mi RNAs T argeting E lements”), negatively regulate Lepr. These i nherited nti‐ L epr miRNAs, also referred (IAL‐miRs), modulate hepatic steatosis, insulin signaling through regulatory Igfbp2, Egfr, Ampk. Furthermore, IAL‐miRs inhibit Ccnd1 not only via binding but Lepr–Igfbp2 axis, contribute hepatocyte senescence. pathological processes interact self‐reinforcing cycle, worsening MetS BPA‐exposed The findings reveal mechanism wherein lipid metabolism reprogramming spermatocytes‐induced perturbations triggered by BPA, leads inheritance suppression axis
Language: Английский