ArticleRedox biology2018
The uremic toxin hippurate promotes endothelial dysfunction via the activation of Drp1-mediated mitochondrial fission.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Animal Models for Studying Protein-Bound Uremic Toxin Removal-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Association of endothelial activation and stress index with all-cause and cardiovascular mortality in patients with diabetic kidney disease: a population-based prospective study.Diabetology & metabolic syndrome · 2026Article
- Chronic Kidney Disease Severity and Risk of Cognitive Impairment.JAMA network open · 2026Article
- Subendocardial Viability Ratio Is Associated With Target Organ Damage and Hints at a Potential Independent Predictor of Cardiovascular Mortality in Older Adults: A Prospective Cohort Study.Journal of the American Heart Association · 2026Observational
- Gut microbiota and serum metabolic profiles in patients with sepsis-induced cardiomyopathy and their association with the disease.Frontiers in cellular and infection microbiology · 2026Article
- The role of AMPK signaling pathway in the pathogenesis of type 2 diabetes mellitus with its complications and related metabolic disorders.Metabolism open · 2025Review
- Gut microbes metabolize strawberry phytochemicals and mediate their beneficial effects on vascular inflammation.Gut microbes · 2025Article
- Mendelian randomization suggests a causal relationship between cerebrospinal fluid metabolites and intracranial aneurysms.Neurosurgical review · 2025Article
- Recharging the Powerhouse: Mitochondrial Dysfunction and Therapy in Cardiorenal Syndrome Type 4.Current heart failure reports · 2025Review
- Select microbial metabolites in the small intestinal lumen regulate vagal activity via receptor-mediated signaling.iScience · 2025Article
- Investigating potential targets of Wulingsan in diabetic nephropathy through network pharmacology and experimental validation.Frontiers in molecular biosciences · 2025Article
- The essential oil from the rhizomes ofFrontiers in pharmacology · 2025Article
- The survival of B cells is compromised in kidney disease.Nature communications · 2024Article
- Role of Uremic Toxins in Vascular Inflammation Associated with Chronic Kidney Disease.Journal of clinical medicine · 2024Article
- Genetically predicted gut bacteria, circulating bacteria-associated metabolites and pancreatic ductal adenocarcinoma: a Mendelian randomisation study.Scientific reports · 2024Article
- Metabolic Pathways Affected in Patients Undergoing Hemodialysis and Their Relationship with Inflammation.International journal of molecular sciences · 2024Article
- Production of Toxins by the Gut Microbiota: The Role of Dietary Protein.Current nutrition reports · 2024Review
- PPARγ agonist alleviates calcium oxalate nephrolithiasis by regulating mitochondrial dynamics in renal tubular epithelial cell.PloS one · 2024Article
- Mitochondrial Impairment: A Link for Inflammatory Responses Activation in the Cardiorenal Syndrome Type 4.International journal of molecular sciences · 2023Review
- The Complex Interplay between Imbalanced Mitochondrial Dynamics and Metabolic Disorders in Type 2 Diabetes.Cells · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The accumulation of uremic toxins in chronic kidney disease (CKD) induces inflammation, oxidative stress and endothelial dysfunction, which is a key step in atherosclerosis. Accumulating evidence indicates increased mitochondrial fission is a contributing mechanism for impaired endothelial function. Hippurate, a uremic toxin, has been reported to be involved in cardiovascular diseases. Here, we assessed the endothelial toxicity of hippurate and the contribution of altered mitochondrial dynamics to hippurate-induced endothelial dysfunction. Treatment of human aortic endothelial cells with hippurate reduced the expression of endothelial nitric oxide synthase (eNOS) and increased the expression of intercellular cell adhesion molecule-1 (ICAM-1) and von Willebrand factor (vWF). The mechanisms of hippurate-induced endothelial dysfunction in vitro depended on the activation of Dynamin-related protein 1 (Drp1)-mediated mitochondrial fission and overproduction of mitochondrial reactive oxygen species (mitoROS). In a rat model in which CKD was induced by 5/6 nephrectomy (CKD rat), we observed increased oxidative stress, impaired endothelium-dependent vasodilation, and elevated soluble biomarkers of endothelial dysfunction (ICAM-1 and vWF). Similarly, endothelial dysfunction was identified in healthy rats treated with disease-relevant concentrations of hippurate. In aortas of CKD rats and hippurate-treated rats, we observed an increase in Drp1 protein levels and mitochondrial fission. Inhibition of Drp1 improved endothelial function in both rat models. These results indicate that hippurate, by itself, can cause endothelial dysfunction. Increased mitochondrial fission plays an active role in hippurate-induced endothelial dysfunction via an increase in mitoROS.
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