ReviewNature reviews. Nephrology2024
Post-translational modifications in kidney diseases and associated cardiovascular risk.
Review in Nature reviews. Nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
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
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.
- Oral Health in Early and Advanced Stages (1-4) of Chronic Kidney Disease: A Systematic Review and Meta-Analysis.International dental journal · 2026Pooled it
- Pooled it
- Association of IgG N-Glycans With Adverse Outcomes in CKD.Kidney international reports · 2026Article
- Sirtuin 1 deficiency mediates chronic kidney disease-induced inflammaging cardiovascular calcification.Molecular biomedicine · 2026Article
- Targeting ADAR1 lactylation activates innate immune and overcomes chemoresistance in ovarian cancer.Cell death and differentiation · 2026Article
- The role of protein prenylation in kidney diseases: Molecular basis and therapeutic implications.Molecular biology reports · 2026Review
- Risedronate attenuates renal fibrosis by targeting prenylation-dependent RhoA/ROCK1 and ERK/NF-κB signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.Frontiers in pharmacology · 2026Review
- Regulatory networks of post-translational modifications in diabetic kidney disease: from pathogenic mechanisms to therapeutic frontiers.Frontiers in endocrinology · 2026Review
- Blood Metabolites Mediate the Effects of Gut Microbiota on Diabetic Nephropathy: A Mendelian Randomization Study.International journal of endocrinology · 2026Article
- A guide to uraemic toxicity.Nature reviews. Nephrology · 2026Review
- Precision Profiling of the Cardiovascular Post-Translationally Modified Proteome.Journal of cardiovascular development and disease · 2026Review
- Glycosylation Profiles in Cardiovascular Diseases: A Bibliometric Analysis.Health data science · 2026Article
- Ten Hot Topics in Cardiovascular Risk Management for Chronic Kidney Disease.Cardiorenal medicine · 2026Review
- Age-associated accumulation of carbamylation-derived products in tissues is independent from the myeloperoxidase pathway in mice.PloS one · 2026Article
- The Physiological Roles and Pathological Implications of Urea Transporters in the Cardiovascular System.Biomedicines · 2025Review
- Sentrin-specific protease 3 (SENP3)-mediated Krüppel-like factor 4 (KLF4) deSUMOylation regulates vascular smooth muscle cell phenotypic switching in atherosclerosis.Molecular biomedicine · 2025Article
- Lactylation modification regulates acute myeloid leukemia pathogenesis and immune microenvironment.Discover oncology · 2025Article
- UBC9-associated SUMOylation contributes to β-catenin activation and kidney fibrosis.Kidney international · 2025Article
- Recent advances in S-palmitoylation and its emerging roles in human diseases.Journal of hematology & oncology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with chronic kidney disease (CKD) are at an increased cardiovascular risk compared with the general population, which is driven, at least in part, by mechanisms that are uniquely associated with kidney disease. In CKD, increased levels of oxidative stress and uraemic retention solutes, including urea and advanced glycation end products, enhance non-enzymatic post-translational modification events, such as protein oxidation, glycation, carbamylation and guanidinylation. Alterations in enzymatic post-translational modifications such as glycosylation, ubiquitination, acetylation and methylation are also detected in CKD. Post-translational modifications can alter the structure and function of proteins and lipoprotein particles, thereby affecting cellular processes. In CKD, evidence suggests that post-translationally modified proteins can contribute to inflammation, oxidative stress and fibrosis, and induce vascular damage or prothrombotic effects, which might contribute to CKD progression and/or increase cardiovascular risk in patients with CKD. Consequently, post-translational protein modifications prevalent in CKD might be useful as diagnostic biomarkers and indicators of disease activity that could be used to guide and evaluate therapeutic interventions, in addition to providing potential novel therapeutic targets.
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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 Socratic graph.