Sodium retention in the nephrotic syndrome and the non-enzymatic function of prostasin
Author:
Publisher
Springer Science and Business Media LLC
Subject
Physiology (medical),Clinical Biochemistry,Physiology
Link
https://link.springer.com/content/pdf/10.1007/s00424-022-02684-w.pdf
Reference10 articles.
1. Andreasen D, Vuagniaux G, Fowler-Jaeger N, Hummler E, Rossier BC (2006) Activation of epithelial sodium channels by mouse channel activating proteases (mCAP) expressed in Xenopus oocytes requires catalytic activity of mCAP3 and mCAP2 but not mCAP1. J Am Soc Nephrol 17:968–976. https://doi.org/10.1681/asn.2005060637
2. Essigke D, Ilyaskin AV, Wörn M, Bohnert BN, Xiao M, Daniel C, Amann K, Birkenfeld AL, Szabo R, Bugge TH, Korbmacher C, Artunc F (2021) Zymogen-locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice. Acta physiologica (Oxford, England) e13640. https://doi.org/10.1111/apha.13640
3. Essigke D, Bohnert BN, Janessa A, Wörn M, Omage K, Kalbacher H, Birkenfeld AL, Bugge TH, Szabo R, Artunc F (2022) Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity. Pflügers Archiv
4. Fila M, Sassi A, Brideau G, Cheval L, Morla L, Houillier P, Walter C, Gennaoui M, Collignon L, Keck M, Planelles G, Bakouh N, Peuchmaur M, Deschênes G, Anegón I, Remy S, Vogt B, Crambert G, Doucet A (2021) A variant of ASIC2 mediates sodium retention in nephrotic syndrome. JCI Insight. https://doi.org/10.1172/jci.insight.148588
5. Hinrichs GR, Jensen BL, Svenningsen P (2020) Mechanisms of sodium retention in nephrotic syndrome. Curr Opin Nephrol Hypertens 29:207–212. https://doi.org/10.1097/mnh.0000000000000578
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