biostudies-literatureTarantini SNational Institute of Neurological Disorders and StrokeNCCIH NIH HHSNIA NIH HHSNINDS NIH HHSNational Center for Complementary and Alternative MedicineNational Institute of General Medical SciencesNational Institute on AgingNIGMS NIH HHS239-258https://www.ebi.ac.uk/biostudies/studies/S-EPMC5061677biostudies-literatureUnknown38(4)Epidemiological findings support the concept of Developmental Origins of Health and Disease, suggesting that early-life hormonal influences during a sensitive period of development have a fundamental impact on vascular health later in life. The endocrine changes that occur during development are highly conserved across mammalian species and include dramatic increases in circulating IGF-1 levels during adolescence. The present study was designed to characterize the effect of developmental IGF-1 deficiency on the vascular aging phenotype. To achieve that goal, early-onset endocrine IGF-1 deficiency was induced in mice by knockdown of IGF-1 in the liver using Cre-lox technology (Igf1 ^f/f mice crossed with mice expressing albumin-driven Cre recombinase). This model exhibits low-circAge (Dordrecht, Netherlands)IGF-1 deficiency in a critical period early in life influences the vascular aging phenotype in mice by altering miRNA-mediated post-transcriptional gene regulation: implications for the developmental origins of health and disease hypothesis.PMC5061677R01 AT006526U54 GM104938NS056218R01 AG038747R01 NS056218AT006526R01 AG055395AG031085P30 AG0509115U54GM104938P30 AG028718R01 AG047879K08 AG031085AG038747Valcarcel-Ares MNTarantini SWei JYSonntag WECsiszar AAshpole NMGiles CBWren JDUngvari ZfalseIGF-1 deficiency in a critical period early in life influences the vascular aging phenotype in mice by altering miRNA-mediated post-transcriptional gene regulation: implications for the developmental origins of health and disease hypothesis.Epidemiological findings support the concept of Developmental Origins of Health and Disease, suggesting that early-life hormonal influences during a sensitive period of development have a fundamental impact on vascular health later in life. The endocrine changes that occur during development are highly conserved across mammalian species and include dramatic increases in circulating IGF-1 levels during adolescence. The present study was designed to characterize the effect of developmental IGF-1 deficiency on the vascular aging phenotype. To achieve that goal, early-onset endocrine IGF-1 deficiency was induced in mice by knockdown of IGF-1 in the liver using Cre-lox technology (Igf1 ^f/f mice crossed with mice expressing albumin-driven Cre recombinase). This model exhibits low-circ2016-01-01T00:00:00Z2016 Aug2025-05-29T19:41:05.376Z2025-05-29T19:41:05.376ZS-EPMC50616772756630810.1007/s11357-016-9943-9