ArticleJournal of the American Heart Association2015
p-Cresyl sulfate aggravates cardiac dysfunction associated with chronic kidney disease by enhancing apoptosis of cardiomyocytes.
Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.
- Pooled it
- Cardiovascular-kidney-metabolic syndrome through the lens of gut‑derived uremic toxins.Gut microbes · 2026Review
- Microbiome-derived metabolites shape CD4+ T cell differentiation and immune aging in HIV-1 infection.JCI insight · 2026Article
- Review
- Review
- Article
- Role of the ABCG2 transporter in the biodistribution of the food-borne uremic toxin p-cresyl sulfate.Scientific reports · 2026Article
- Multi-Species Synbiotic Supplementation After Antibiotics Promotes Recovery of Microbial Diversity and Function, and Increases Gut Barrier Integrity: A Randomized, Placebo-Controlled Trial.Antibiotics (Basel, Switzerland) · 2026Article
- The Role and Mechanism of Gut Microbiota and Metabolites in Vascular Calcification.International journal of molecular sciences · 2026Review
- Microbiome-Derived Metabolites Shape CD4bioRxiv : the preprint server for biology · 2026Article
- The gut-heart axis in heart failure: from bidirectional pathophysiological mechanisms to integrative therapeutic strategies.Frontiers in microbiology · 2026Review
- Review
- Sex-specific cardiac dysfunction in mice with chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Article
- The Non-Traditional Cardiovascular Culprits in Chronic Kidney Disease: Mineral Imbalance and Uremic Toxin Accumulation.International journal of molecular sciences · 2025Review
- Microbial Metabolites and Cardiovascular Dysfunction: A New Era of Diagnostics and Therapy.Cells · 2025Review
- The gut microbiome connects nutrition and human health.Nature reviews. Gastroenterology & hepatology · 2025Review
- Gut Dysbiosis and Probiotic Therapy in Chronic Kidney Disease: A Comprehensive Review.Probiotics and antimicrobial proteins · 2025Review
- Renal-Cardiac Crosstalk in the Pathogenesis and Progression of Heart Failure.Circulation research · 2025Review
- Gut microbiome remodeling in chronic kidney disease: implications of kidney replacement therapies and therapeutic interventions.Frontiers in medicine · 2025Review
- Advances in kidney disease: pathogenesis and therapeutic targets.Frontiers in medicine · 2025Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiovascular disease is the leading cause of death in patients with chronic kidney disease. A body of evidence suggests that p-cresyl sulfate (PCS), a uremic toxin, is associated with the cardiovascular mortality rate of patients with chronic kidney disease; however, the molecular mechanisms underlying this feature have not yet been fully elucidated. METHODS AND
resultsWe aimed to determine whether PCS accumulation could adversely affect cardiac dysfunction via direct cytotoxicity to cardiomyocytes. In mice that underwent 5/6 nephrectomy, PCS promoted cardiac apoptosis and affected the ratio of left ventricular transmitral early peak flow velocity to left ventricular transmitral late peak flow velocity (the E/A ratio) observed by echocardiography (n=8 in each group). Apocynin, an inhibitor of NADPH oxidase activity, attenuates this alteration of the E/A ratio (n=6 in each group). PCS also exhibited proapoptotic properties in H9c2 cells by upregulating the expression of p22(phox) and p47(phox), NADPH oxidase subunits, and the production of reactive oxygen species. Apocynin and N-acetylcysteine were both able to suppress the effect of PCS, underscoring the importance of NADPH oxidase activation for the mechanism of action.
conclusionsThis study demonstrated that the cardiac toxicity of PCS is at least partially attributed to induced NADPH oxidase activity and reactive oxygen species production facilitating cardiac apoptosis and resulting in diastolic dysfunction.
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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.