F-53B-induced placental vascular endothelial dysfunction leads to intrauterine growth retardation of fetal mice

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Experimental analysis reveals fetal growth retardation in mice exposed to F-53B, indicating vascular injury's role in developmental toxicity.

F-53B exposure prompts significant fetal growth retardation in a controlled in vivo model, indicating toxicity.
Mice administered with F-53B showed notable vascular injury and altered placental function due to increased permeability and reduced blood flow.
Analysis involved RNA sequencing and trophoblast-endothelial co-culture to uncover mechanisms behind observed growth impacts.
These findings highlight a critical link between F-53B exposure and developmental toxicity through vascular mechanisms in placental function.

Guo et al. (2025) studied this question.

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View Full Paper

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Authors

Experimental analysis reveals fetal growth retardation in mice exposed to F-53B, indicating vascular injury's role in developmental toxicity.

F-53B exposure prompts significant fetal growth retardation in a controlled in vivo model, indicating toxicity.
Mice administered with F-53B showed notable vascular injury and altered placental function due to increased permeability and reduced blood flow.
Analysis involved RNA sequencing and trophoblast-endothelial co-culture to uncover mechanisms behind observed growth impacts.
These findings highlight a critical link between F-53B exposure and developmental toxicity through vascular mechanisms in placental function.

Guo et al. (2025) studied this question.

View Full Paper

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Bookmark