ArticleActa physiologica (Oxford, England)2021
Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome.
Article in Acta physiologica (Oxford, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Urokinase Promotes Redundantly Intratubular C3a-Formation But Not ENaC-Driven Hypertension in DOCA/Salt Kidney Injury.Hypertension (Dallas, Tex. : 1979) · 2026Article
- Activation of the alternative complement pathway and its relevance for sodium retention in experimental nephrotic syndrome.Pflugers Archiv : European journal of physiology · 2026Article
- Rather a versatile multi-tool than a sword: an integral role of the plasminogen system in health and disease.Frontiers in immunology · 2026Review
- Resistance to doxorubicin-induced proteinuria and proteolytic activation of ENaC in 129S2/SvPas mice.Physiological reports · 2025Article
- The enigma of ENaC activation by proteolytic cleavage: a never ending quest?Pflugers Archiv : European journal of physiology · 2025Article
- Loss of the alpha subunit distal furin cleavage site blunts ENaC activation following NaThe Journal of physiology · 2024Article
- Epithelial NaComprehensive Physiology · 2024Review
- Activation of renal epithelial NaFrontiers in pediatrics · 2024Article
- A Serine Protease Inhibitor, Camostat Mesilate, Suppresses Urinary Plasmin Activity and Alleviates Hypertension and Podocyte Injury in Dahl Salt-Sensitive Rats.International journal of molecular sciences · 2023Article
- Kidney-Specific CAP1/Prss8-Deficient Mice Maintain ENaC-Mediated Sodium Balance through an Aldosterone Independent Pathway.International journal of molecular sciences · 2022Article
- Sodium retention in nephrotic syndrome is independent of the activation of the membrane-anchored serine protease prostasin (CAP1/PRSS8) and its enzymatic activity.Pflugers Archiv : European journal of physiology · 2022Article
- ENaC activation by proteases.Acta physiologica (Oxford, England) · 2022Review
- Essential role of DNA-PKcs and plasminogen for the development of doxorubicin-induced glomerular injury in mice.Disease models & mechanisms · 2021Article
- 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) · 2021Article
- Cleavage state of γENaC in mouse and rat kidneys.American journal of physiology. Renal physiology · 2021Article
- The Deleterious Effects of Impaired Fibrinolysis on Skeletal Development Are Dependent on Fibrin(ogen), but Independent of Interlukin-6.Frontiers in cardiovascular medicine · 2021Article
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
aimSodium retention is the hallmark of nephrotic syndrome (NS) and mediated by the proteolytic activation of the epithelial sodium channel (ENaC) by aberrantly filtered serine proteases. Plasmin is highly abundant in nephrotic urine and has been proposed to be the principal serine protease responsible for ENaC activation in NS. However, a proof of the essential role of plasmin in experimental NS is lacking.
methodsWe used a genetic mouse model of NS based on an inducible podocin knockout (Bl6-Nphs2
resultsUninduced nphs2
conclusionsThis 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.
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