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ABSTRACT: Background
Congenital diseases of the urinary tract are frequently observed in infants. Such diseases present a number of developmental anomalies such as hydroureter and hydronephrosis. Although some genetically-modified mouse models of growth factor signaling genes reproduce urinary phenotypes, the pathogenic mechanisms remain obscure. Previous studies suggest that a portion of the cells in the external genitalia and bladder are derived from peri-cloacal mesenchymal cells that receive Hedgehog (Hh) signaling in the early developmental stages. We hypothesized that defects in such progenitor cells, which give rise to urinary tract tissues, may be a cause of such diseases.Methodology/principal findings
To elucidate the pathogenic mechanisms of upper urinary tract malformation
SUBMITTER: Haraguchi R
PROVIDER: S-EPMC3408458 | biostudies-literature | 2012
REPOSITORIES: biostudies-literature