ArticleAntioxidants (Basel, Switzerland)2020
Hippuric Acid Promotes Renal Fibrosis by Disrupting Redox Homeostasis via Facilitation of NRF2-KEAP1-CUL3 Interactions in Chronic Kidney Disease.
Article in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 79 citations in OpenAlex.
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- Serum metabolic fingerprinting for diagnosis and therapeutic applications of ovarian endometriosis.iScience · 2026Article
- Comparative Study of Redox Status of MDCK Cells in Chicken Embryo Extract Versus Fetal Bovine Serum.International journal of molecular sciences · 2026Article
- Aromatic microbial metabolite hippuric acid enhances inflammatory responses in macrophages via TLR-MyD88 signaling and lipid remodeling.Cell reports · 2026Article
- Gut microbiota and metabolomics reveal the combined effects ofFrontiers in pharmacology · 2026Article
- Review
- Impact of gut microbiota in chronic kidney disease: natural polyphenols as beneficial regulators.Renal failure · 2025Review
- Monitoring of Allograft Adaptation After Kidney Transplantation in Pediatric Patients by Targeted Plasma Metabolomics.International journal of molecular sciences · 2025Article
- Spatial metabolic and phenotypic characterization of the germ-free mouse model.Annals of the New York Academy of Sciences · 2025Article
- NRF2 Dysregulation and Therapeutic Insights Across Chronic Kidney Diseases.International journal of molecular sciences · 2025Review
- ELANE enhances KEAP1 protein stability and reduces NRF2-mediated ferroptosis inhibition in metabolic dysfunction-associated fatty liver disease.Cell death & disease · 2025Article
- The spatiotemporal and paradoxical roles of NRF2 in renal toxicity and kidney diseases.Redox biology · 2025Review
- Metabolomic and Lipidomic Profiling for Pre-Transplant Assessment of Delayed Graft Function Risk Using Chemical Biopsy with Microextraction Probes.International journal of molecular sciences · 2024Article
- Identification of serum biomarkers for chronic kidney disease using serum metabolomics.Renal failure · 2024Article
- Genetically predicted gut bacteria, circulating bacteria-associated metabolites and pancreatic ductal adenocarcinoma: a Mendelian randomisation study.Scientific reports · 2024Article
- P4HB regulates the TGFβ/SMAD3 signaling pathway through PRMT1 to participate in high glucose-induced epithelial-mesenchymal transition and fibrosis of renal tubular epithelial cells.BMC nephrology · 2024Article
- Metabolic Pathways Affected in Patients Undergoing Hemodialysis and Their Relationship with Inflammation.International journal of molecular sciences · 2024Article
- Gut microbiota dysbiosis in hyperuricaemia promotes renal injury through the activation of NLRP3 inflammasome.Microbiome · 2024Article
- Multi-Omic Analysis Reveals Genetic Determinants and Therapeutic Targets of Chronic Kidney Disease and Kidney Function.International journal of molecular sciences · 2024Article
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7 authors at 1 institution in 1 country.
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Abstract
Chronic kidney disease (CKD) is characterized by the accumulation of protein-bound uremic toxins (PBUTs), which play a pathophysiological role in renal fibrosis (a common pathological process resulting in CKD progression). Accumulation of the PBUT hippuric acid (HA) is positively correlated with disease progression in CKD patients, suggesting that HA may promote renal fibrosis. Oxidative stress is the most important factor affecting PBUTs nephrotoxicity. Herein, we assessed the ability of HA to promote kidney fibrosis by disrupting redox homeostasis. In HK-2 cells, HA increased fibrosis-related gene expression, extracellular matrix imbalance, and oxidative stress. Additionally, reactive oxygen species (ROS)-mediated TGFβ/SMAD signaling contributed to HA-induced fibrotic responses. HA disrupted antioxidant networks by decreasing the levels of nuclear factor erythroid 2-related factor 2 (NRF2), leading to ROS accumulation and fibrotic responses, as evidenced by NRF2 activation and knockdown. Moreover, NRF2 levels were reduced by NRF2 ubiquitination, which was regulated via increased interactions of Kelch-like ECH-associated protein 1 with Cullin 3 and NRF2. Finally, renal fibrosis and redox imbalance promoted by HA were confirmed in rats. Importantly, sulforaphane (NRF2 activator) reversed HA-promoted renal fibrosis. Thus, HA promotes renal fibrosis in CKD by disrupting NRF2-driven antioxidant system, indicating that NRF2 is a potential therapeutic target for CKD.
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