ArticleCurrent research in toxicology2025
GenX induces offspring vascular endothelial ferroptosis by targeting GPX4 for ubiquitination-dependent degradation.
Article in Current research in toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
GenX, a widely used replacement for PFOA, has become ubiquitously distributed in aquatic ecosystems, soil, and biota, yet its developmental toxicity in offspring is poorly characterized. This study delineates the intergenerational vascular consequences of gestational GenX exposure. Pregnant mice exposed to GenX exhibited adverse pregnancy outcomes, notably fetal growth restriction and placental structural impairment. Pathological evaluation demonstrated labyrinthine zone disorganization and diminished Occludin expression in placentas, indicating disrupted barrier function that likely facilitates maternal-fetal GenX transfer. Critically, exposed offspring displayed systemic vascular maldevelopment, marked by aberrant angiogenesis and endothelial dysfunction. Mechanistic investigations revealed that GenX provoked ferroptosis in vascular endothelial cells, evidenced by depleted GSH, suppressed SOD activity, elevated MDA and Fe
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