ArticleInflammation2019
Amelioration of Lipopolysaccharide-Induced Nephrotic Proteinuria by NFAT5 Depletion Involves Suppressed NF-κB Activity.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Evaluation of serum miR-122-5p, miR-486-5p, miR-21-5p, and their interplay with inflammatory markers in diabetic nephropathy: a case control study.BMC nephrology · 2025Article
- Microglial NFAT5 aggravates neuroinflammation via mediating NLRP6 inflammasome in experimental ischemic stroke.Genes & diseases · 2025Article
- Unlocking the therapeutic potential of the NFAT pathway in kidney diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- LDP alleviates TKI-induced proteinuria through reversing the expression of RelA in renal tissues.Frontiers in medicine · 2023Article
- miRNA-486-5p: signaling targets and role in non-malignant disease.Cellular and molecular life sciences : CMLS · 2022Review
- An Integration of Network Pharmacology and Experimental Verification to Investigate the Mechanism of Guizhi to Treat Nephrotic Syndrome.Frontiers in pharmacology · 2021Article
- The evolving role of TonEBP as an immunometabolic stress protein.Nature reviews. Nephrology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Idiopathic nephrotic syndrome (INS) is characterized by proteinuria, in which podocyte dysfunction associated with NF-κB-mediated inflammation plays an important role. The nuclear factor of activated T cells 5 (NFAT5) has been shown to enhance NF-κB activity. However, whether NFAT5 is associated with proteinuria remains uncharacterized. NFAT5 is upregulated in the glomeruli in lipopolysaccharide (LPS)-induced mouse nephrotic proteinuria, as well as in LPS-treated podocytes in vitro. In addition, NFAT5 depletion improves filtration barrier function of LPS-treated podocytes in vitro. Mechanistically, NFAT5 depletion suppresses NF-κB activation and downstream proinflammatory reaction in LPS-treated podocytes, and moreover, NF-κB inhibition improves filtration barrier function of LPS-treated podocytes, suggesting that the suppressed NF-κB activity at least partly accounts for NFAT5 depletion-improved filtration barrier function. Furthermore, in vivo, depletion of NFAT5 suppresses NF-κB activity and ameliorates nephrotic proteinuria in LPS-treated mice. These findings suggest a protective role of NFAT5 depletion against LPS-induced nephrotic proteinuria and relate it to the suppression of NF-κB activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.