Low-activity programming of the PDGFR β/FAK pathway mediates H-type vessel dysplasia and high susceptibility to osteoporosis in female offspring rats after prenatal dexamethasone exposure.

This study enhances the understanding of the molecular mechanism of dexamethasone-induced bone development toxicity and provides new insights for exploring the early intervention and therapeutic targets of foetal-derived osteoporosis.
PMID: 33434537 [PubMed - as supplied by publisher]

Source: Biochemical Pharmacology - January 9, 2021 Category: Drugs & Pharmacology Authors: Shangguan Y, Wu Z, Xie X, Zhou S, He H, Xiao H, Liu L, Zhu J, Chen H, Han H, Wang H, Chen L Tags: Biochem Pharmacol Source Type: research