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Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome.

Mengyun XiaoBernhard N BohnertHande AypekOliver KretzFlorian GrahammerUte AukschunMatthias WörnAndrea JanessaDaniel EssigkeChristoph DanielKerstin AmannTobias B HuberEdward F PlowAndreas L BirkenfeldFerruh Artunc
Published in: Acta physiologica (Oxford, England) (2020)
This study shows that mice lacking urinary plasminogen are not protected from ENaC-mediated sodium retention in experimental NS. This points to an essential role of other urinary serine proteases in the absence of plasminogen.
Keyphrases
  • mouse model
  • genome wide
  • high fat diet induced
  • gene expression
  • adipose tissue