ArticleJournal of cellular and molecular medicine2020
Up-regulation of HDACs, a harbinger of uraemic endothelial dysfunction, is prevented by defibrotide.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Defibrotide for Protecting Against and Managing Endothelial Injury in Hematologic Malignancies and COVID-19.Biomolecules · 2025Review
- Epigenetic regulation in coronary artery disease: from mechanisms to emerging therapies.Frontiers in molecular biosciences · 2025Review
- Review
- Molecular cross-talk between long COVID-19 and Alzheimer's disease.GeroScience · 2024Review
- Trichostatin D as a Novel KLF2 Activator Attenuates TNFα-Induced Endothelial Inflammation.International journal of molecular sciences · 2022Article
- Identification of core genes and pathways between geriatric multimorbidity and renal insufficiency: potential therapeutic agents discovered using bioinformatics analysis.BMC medical genomics · 2022Article
- HDAC1: an environmental sensor regulating endothelial function.Cardiovascular research · 2022Review
- Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials.Signal transduction and targeted therapy · 2022Review
- Is the Endothelium the Missing Link in the Pathophysiology and Treatment of COVID-19 Complications?Cardiovascular drugs and therapy · 2022Review
- Correlation analysis between expression of histone deacetylase 6 and clinical parameters in IgA nephropathy patients.Renal failure · 2021Article
- Applying Proteomics and Integrative "Omics" Strategies to Decipher the Chronic Kidney Disease-Related Atherosclerosis.International journal of molecular sciences · 2021Review
- Role of PI3K in the Progression and Regression of Atherosclerosis.Frontiers in pharmacology · 2021Review
- The induction strategies administered in the treatment of multiple myeloma exhibit a deleterious effect on the endothelium.Bone marrow transplantation · 2020Article
- Up-regulation of HDACs, a harbinger of uraemic endothelial dysfunction, is prevented by defibrotide.Journal of cellular and molecular medicine · 2020Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial dysfunction is an earlier contributor to the development of atherosclerosis in chronic kidney disease (CKD), in which the role of epigenetic triggers cannot be ruled out. Endothelial protective strategies, such as defibrotide (DF), may be useful in this scenario. We evaluated changes induced by CKD on endothelial cell proteome and explored the effect of DF and the mechanisms involved. Human umbilical cord vein endothelial cells were exposed to sera from healthy donors (n = 20) and patients with end-stage renal disease on haemodialysis (n = 20). Differential protein expression was investigated by using a proteomic approach, Western blot and immunofluorescence. HDAC1 and HDAC2 overexpression was detected. Increased HDAC1 expression occurred at both cytoplasm and nucleus. These effects were dose-dependently inhibited by DF. Both the HDACs inhibitor trichostatin A and DF prevented the up-regulation of the endothelial dysfunction markers induced by the uraemic milieu: intercellular adhesion molecule-1, surface Toll-like receptor-4, von Willebrand Factor and reactive oxygen species. Moreover, DF down-regulated HDACs expression through the PI3/AKT signalling pathway. HDACs appear as key modulators of the CKD-induced endothelial dysfunction as specific blockade by trichostatin A or by DF prevents endothelial dysfunction responses to the CKD insult. Moreover, DF exerts its endothelial protective effect by inhibiting HDAC up-regulation likely through PI3K/AKT.
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