ReviewCells2020
Molecular Mechanisms Underlying the Cardiovascular Toxicity of Specific Uremic Solutes.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Safety and Efficacy of CYP2C19 Genotype-Guided Escalation of P2YCardiovascular drugs and therapy · 2024Trial
- Cardiovascular Risk Comparison between Expanded Hemodialysis Using Theranova and Online Hemodiafiltration (CARTOON): A Multicenter Randomized Controlled Trial.Scientific reports · 2021Trial
- Development of a nomogram for predicting incident heart failure and all-cause mortality in patients with chronic kidney disease: a 3-year follow-up study.Frontiers in medicine · 2026Article
- Unveiling the role of sex in the metabolism of indoxyl sulfate and apixaban.Scientific reports · 2025Article
- The Perspectives of Platelet Proteomics in Health and Disease.Biomedicines · 2024Review
- Natural antagonistic flavones for AhR inhibit indoxyl sulfate-induced inflammatory gene expressionFood & nutrition research · 2024Article
- Uremic Toxins Induce THP-1 Monocyte Endothelial Adhesion and Migration through Specific miRNA Expression.International journal of molecular sciences · 2023Article
- Integrated metabolomics and proteomics reveal biomarkers associated with hemodialysis in end-stage kidney disease.Frontiers in pharmacology · 2023Article
- Markers of Kidney Tubular Secretion and Risk of Adverse Events in SPRINT Participants with CKD.Journal of the American Society of Nephrology : JASN · 2022Article
- [Gut-derived uremic toxin trimethylamine-N-oxide in cardiovascular disease under end-stage renal disease: an injury mechanism and therapeutic target].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2022Review
- Serum Orotidine: A Novel Biomarker of Increased CVD Risk in Type 2 Diabetes Discovered Through Metabolomics Studies.Diabetes care · 2022Article
- Tryptophan metabolites suppress the Wnt pathway and promote adverse limb events in chronic kidney disease.The Journal of clinical investigation · 2022Article
- Article
- Effect of Vancomycin on the Gut Microbiome and Plasma Concentrations of Gut-Derived Uremic Solutes.Kidney international reports · 2021Article
- Proteomics: A Tool to Study Platelet Function.International journal of molecular sciences · 2021Review
- Toxin Removal and Inflammatory State Modulation during Online Hemodiafiltration Using Two Different Dialyzers (TRIAD2 Study).Methods and protocols · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mounting evidence strongly suggests a causal link between chronic kidney disease (CKD) and cardiovascular disease (CVD). Compared with non-CKD patients, patients with CKD suffer disproportionately from CVD and derive suboptimal benefits from interventions targeting conventional CVD risk factors. Uremic toxins (UTs), whose plasma levels rapidly rise as CKD progresses, represent a unique risk factor in CKD, which has protean manifestations on CVD. Among the known UTs, tryptophan metabolites and trimethylamine N-oxide are well-established cardiovascular toxins. Their molecular mechanisms of effect warrant special consideration to draw translational value. This review surveys current knowledge on the effects of specific UTs on different pathways and cell functions that influence the integrity of cardiovascular health, with implication for CVD progression. The effect of UTs on cardiovascular health is an example of a paradigm in which a cascade of molecular and metabolic events induced by pathology in one organ in turn induces dysfunction in another organ. Deciphering the molecular mechanisms underlying such cross-organ pathologies will help uncover therapeutic targets to improve the management of CVD in patients with CKD.
Indexed as
Identifiers
What OpenQuestion holds
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.