ArticleFrontiers in physiology2019
Inhibition of IL-1β by Aliskiren Improved Renal AQP2 Expression and Urinary Concentration Defect in Ureteral Obstruction and Release.
Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 12 citations in OpenAlex.
- An Exploratory Analysis of Potential Core Targets and Signaling Pathways Linking Dexmedetomidine to Diabetes Insipidus: Integration of FAERS Pharmacovigilance Data, Network Toxicology and Clinical Transcriptomics.Drug design, development and therapy · 2026Article
- Lysine acetylation of aquaporin-3 promotes water permeability but is not essential for urine concentrating ability.American journal of physiology. Renal physiology · 2025Article
- Abnormal urodynamic changes in post-upper urinary tract dysfunction in ureteral obstruction rat models.Frontiers in physiology · 2024Article
- β-sitosterol alleviates dextran sulfate sodium-induced experimental colitis via inhibition of NLRP3/Caspase-1/GSDMD-mediated pyroptosis.Frontiers in pharmacology · 2023Article
- Hesperetin from Root Extract ofInternational journal of molecular sciences · 2022Article
- Glucocorticoid Receptor Maintains Vasopressin Responses in Kidney Collecting Duct Cells.Frontiers in physiology · 2022Article
- The long-term renal effects of short periods of unilateral ureteral obstruction.International journal of physiology, pathophysiology and pharmacology · 2022Review
- A primitive type of renin-expressing lymphocyte protects the organism against infections.Scientific reports · 2021Article
- Statins ameliorate cholesterol-induced inflammation and improve AQP2 expression by inhibiting NLRP3 activation in the kidney.Theranostics · 2020Article
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10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously demonstrated that ureteral obstruction is associated with a urinary concentrating defect and reduced expression of renal aquaporins (AQPs), in which the renin-angiotensin system (RAS) may play an important role. The aims of the present study were to examine whether the renin inhibitor aliskiren could prevent the reduction in AQP expression and improve the urinary concentrating capacity in mice with bilateral ureteral obstruction (BUO) and BUO release. BUO was performed for 24 h, and BUO release was performed for 1 (B-R1D) or 3 days (B-R3D) with or without aliskiren treatment. Aliskiren prevented polyuria and decreased urine osmolality induced by B-R3D. In mice with BUO and BUO release, aliskiren attenuated the reduction in AQP2 protein and mRNA expression in the obstructed kidneys. B-R3D increased the protein expression of NLRP3 inflammasome components ASC, caspase-1, and interleukin-1β in the obstructed kidneys, which was markedly prevented by aliskiren. Moreover, the NF-κB inhibitor Bay 11-7082 blocked NLRP3 inflammasome activation and attenuated the decrease in AQP2 protein expression in primary cultured rat inner medullary collecting duct cells treated with angiotensin II. These results indicate that the renin inhibitor aliskiren increases water channel AQP2 expression at least partially by suppressing NLRP3 inflammasome activation in the obstructed kidneys of mice with BUO and BUO release.
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