Urokinase-type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)-mediated sodium retention in experimental nephrotic syndrome.
Bernhard N BohnertSophie DaimingerMatthias WörnFlorian SureTobias StaudnerAlexandr V IlyaskinFiras BatboutaAndrea JanessaJonas C SchneiderDaniel EssigkeSandip KanseSilke HaerteisChristoph KorbmacherFerruh ArtuncPublished in: Acta physiologica (Oxford, England) (2019)
uPA is responsible for the conversion of aberrantly filtered plasminogen to plasmin in the tubular lumen in vivo. However, uPA-dependent plasmin generation is not essential for ENaC-mediated sodium retention in experimental nephrotic syndrome.