ReviewAdvances in chronic kidney disease2019
The Role of Nonenzymatic Post-translational Protein Modifications in Uremic Vascular Calcification.
Review in Advances in chronic kidney disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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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.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Complement Activation by Post-Translationally Modified Proteins: Links to Chronic Inflammation and Autoimmunity.Immunological reviews · 2026Review
- [Elevated advanced glycation endproducts is a risk factor for stenosis after primary arteriovenous fistula surgery].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- What is the role of the neutrophil extracellular traps in the cardiovascular disease burden associated with hemodialysis bioincompatibility?Frontiers in medicine · 2023Review
- Protein-bound calcium phosphate in uremic rat serum: a quantitative study.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Considerable technological advances have enabled the identification and linkage of nonenzymatic post-translationally modified proteins to the pathogenesis of cardiovascular disease (CVD) in patients with kidney failure. Through processes such as the nonenzymatic carbamylation reaction as well as the formation of advanced glycation end products, we now know that protein modifications are invariably associated with the development of CVD beyond a mere epiphenomenon and this has become an important focus of nephrology research in recent years. Although the specific mechanisms by which protein modifications occurring in kidney failure that may contribute to CVD are diverse and include pathways such as inflammation and fibrosis, vascular calcification has emerged as a distinct pathological sequelae of protein modifications. In this review, we consider the biological mechanisms and clinical relevance of protein carbamylation and advanced glycation end products in CVD development with a focus on vascular calcification.
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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.