ArticleComputational and structural biotechnology journal2020
Microvesicles from indoxyl sulfate-treated endothelial cells induce vascular calcification
Article in Computational and structural biotechnology journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Redox Network Failure in Chronic Kidney Disease: Hydrogen Sulfide Deficiency, Reactive Sulfur Species Dysregulation and the Uremic Toxin-AhR-Mitochondrial Axis.Antioxidants (Basel, Switzerland) · 2026Review
- Advancing Extracellular Vesicle Research: A Review of Systems Biology and Multiomics Perspectives.Proteomics · 2026Review
- The dual role of extracellular vesicles in vascular calcification: from molecular mechanisms to clinical translation.Frontiers in cardiovascular medicine · 2026Review
- Circulating Extracellular Vesicles as Putative Mediators of Cardiovascular Disease in Paediatric Chronic Kidney Disease.Journal of extracellular vesicles · 2025Article
- Extracellular Vesicles as Mediators of Endothelial Dysfunction in Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- The relationship between programmed cell death and vascular calcification.Frontiers in cardiovascular medicine · 2025Review
- Role of Uremic Toxins in Vascular Inflammation Associated with Chronic Kidney Disease.Journal of clinical medicine · 2024Article
- Article
- Sox9 Accelerates Vascular Aging by Regulating Extracellular Matrix Composition and Stiffness.Circulation research · 2024Article
- Magnesium and Vascular Calcification in Chronic Kidney Disease: Current Insights.International journal of molecular sciences · 2024Review
- The functional role of cellular senescence during vascular calcification in chronic kidney disease.Frontiers in endocrinology · 2024Review
- Epigallocatechin gallate (EGCG) modulates senescent endothelial cell-monocyte communication in age-related vascular inflammation.Frontiers in cardiovascular medicine · 2024Article
- Relationship between Serum Indoxyl Sulfate and Klotho Protein and Vascular Calcification in Patients with Chronic Kidney Disease Stages 3-5.International journal of endocrinology · 2024Article
- Similarities and Differences of Vascular Calcification in Diabetes and Chronic Kidney Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Vascular calcification: from the perspective of crosstalk.Molecular biomedicine · 2023Review
- SLC22A11 Inserts the Uremic Toxins Indoxyl Sulfate and P-Cresol Sulfate into the Plasma Membrane.International journal of molecular sciences · 2023Article
- Extracellular Vesicles as "Very Important Particles" (VIPs) in Aging.International journal of molecular sciences · 2023Review
- Pathogenesis of Chronic Kidney Disease Is Closely Bound up with Alzheimer's Disease, Especially via the Renin-Angiotensin System.Journal of clinical medicine · 2023Review
- Extracellular Vesicles and Vascular Inflammation.Advances in experimental medicine and biology · 2023Article
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular calcification (VC), an unpredictable pathophysiological process and critical event in patients with cardiovascular diseases (CVDs), is the leading cause of morbi-mortality and disability in chronic kidney disease (CKD) patients worldwide. Currently, no diagnostic method is available for identifying patients at risk of VC development; the pathology is detected when the process is irreversible. Extracellular vesicles (EVs) from endothelial cells might promote VC. Therefore, their evaluation and characterization could be useful for designing new diagnostic tools. The aim of the present study is to investigate whether microvesicles (MVs) from endothelial cells damaged by uremic toxin and indoxyl sulfate (IS) could induce calcification in human vascular smooth muscle cells (VMSCs). Besides, we have also analyzed the molecular mechanisms by which these endothelial MVs can promote VC development. Endothelial damage has been evaluated according to the percentage of senescence in endothelial cells, differential microRNAs in endothelial cells, and the amount of MVs released per cell. To identify the role of MVs in VC, VSMCs were treated with MVs from IS-treated endothelial cells. Calcium, inflammatory gene expression, and procalcification mediator levels in VSMCs were determined. IS-treated endothelial cells underwent senescence and exhibited modulated microRNA expression and an increase in the release of MVs. VSMCs exposed to these MVs modulated the expression of pro-inflammatory genes and some mediators involved in calcification progression. MVs produced by IS-treated endothelial cells promoted calcification in VSMCs.
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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.