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ABSTRACT: Rationale
Hypertension prevalence is much higher among children and adolescents with low birth weight and greater postnatal weight gain than in individuals with normal birth weight. However, the cause and molecular mechanisms underlying this complication remain largely unknown. Our previous studies have shown that RGC-32 (response gene to complement 32)-deficient (RGC-32-/-) mice are born significantly smaller but grow faster than their WT (wild type) controls, which allows adult RGC-32-/- mice to attain body weights similar to those of control mice.Objective
The objective of this study is to determine whether RGC-32-/- mice develop hypertension, and if so, to elucidate the underlying mechanisms.Methods and results
By using a radiote
SUBMITTER: Tang JM
PROVIDER: S-EPMC6214659 | biostudies-literature | 2018 Oct
REPOSITORIES: biostudies-literature