Cathepsin B increases ENaC activity leading to hypertension early in nephrotic syndrome.
Amiloride
/ pharmacology
Animals
Cathepsin B
/ antagonists & inhibitors
Epithelial Sodium Channel Blockers
/ pharmacology
Epithelial Sodium Channels
/ metabolism
Glomerulosclerosis, Focal Segmental
/ enzymology
Hypertension
/ etiology
Intracellular Signaling Peptides and Proteins
/ genetics
Kidney Tubules
/ cytology
Lysosomes
/ enzymology
Membrane Proteins
/ genetics
Mice
Mice, Transgenic
Nephrotic Syndrome
/ complications
Proteinuria
/ metabolism
Proteolysis
Sodium
/ metabolism
epithelial sodium channel
focal segmental glomerulosclerosis
hypertension
nephrotic syndrome
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
28
01
2019
revised:
04
04
2019
accepted:
06
05
2019
pubmed:
2
8
2019
medline:
26
9
2020
entrez:
2
8
2019
Statut:
ppublish
Résumé
The NPHS2 gene, encoding the slit diaphragm protein podocin, accounts for genetic and sporadic forms of nephrotic syndrome (NS). Patients with NS often present symptoms of volume retention, such as oedema formation or hypertension. The primary dysregulation in sodium handling involves an inappropriate activation of the epithelial sodium channel, ENaC. Plasma proteases in a proteinuria-dependent fashion have been made responsible; however, referring to the timeline of symptoms occurring and underlying mechanisms, contradictory results have been published. Characterizing the mouse model of podocyte inactivation of NPHS2 (Nphs2
Identifiants
pubmed: 31368174
doi: 10.1111/jcmm.14387
pmc: PMC6787568
doi:
Substances chimiques
Epithelial Sodium Channel Blockers
0
Epithelial Sodium Channels
0
Intracellular Signaling Peptides and Proteins
0
Membrane Proteins
0
NPHS2 protein
0
Scnn1a protein, mouse
0
Scnn1b protein, mouse
0
Scnn1g protein, mouse
0
Amiloride
7DZO8EB0Z3
Sodium
9NEZ333N27
Cathepsin B
EC 3.4.22.1
Ctsb protein, mouse
EC 3.4.22.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
6543-6553Informations de copyright
© 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
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