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Backgrounds And Purposes: Patients with chronic kidney disease (CKD) have higher risk of developing cardiovascular disease. In CKD patients the mechanisms involved in, endothelial damage and the role of different drugs used on these patients are not completely understood. The aim of this work is to analyze the effect of statins and platelet antiaggregant (PA) on endothelial microvesicles (EMVs) and other markers of endothelial dysfunction.
Experimental Approach: Cross-sectional study of 41 patients with CKD 3b-4 and 8 healthy volunteers. Circulating levels of EMVs, vascular endothelial growth factor (VEGF), and advance oxidized protein products (AOPPS) were quantified and the correlation with different comorbidity variables and therapeutic strategies were evaluated.
Results: EMVs are increased in CKD patients as compared with controls (171.1 vs. 68.3/μl, P<.001). It was observed a negative correlation between age and EMVs. Statins and PA were associated with a reduction in EMVs and VEGF levels, independently of the serum total cholesterol levels (TC). The levels of AOPPS and VEGF were not different in CKD vs. controls.
Conclusion: CKD is associated with a change in EMVs, VEGF and AOPP levels. The treatment with statins and PA normalizes these values to almost the observed in controls and this effect is independently of the prevailing TC level. These findings explain the existence of the pleiotropic effects of statins and PA which deserve further studies.
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http://dx.doi.org/10.1016/j.nefro.2018.11.001 | DOI Listing |
Diabetes Obes Metab
September 2025
Department of Pharmacy, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
Background: Diabetic retinopathy (DR) is a major complication of diabetes mellitus, characterised by retinal vasculopathy and oxidative stress. Semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), has demonstrated cardiovascular benefits but has also been associated with mixed effects on DR progression. This study investigates the potential of semaglutide to attenuate DR progression by ameliorating retinal vasculopathy and oxidative stress in both in vivo and in vitro models.
View Article and Find Full Text PDFMol Syst Biol
September 2025
Department of Medicine, Division of Cardiovascular Medicine, Stanford University, Stanford, CA, USA.
Vascular sites have distinct susceptibility to atherosclerosis and aneurysm, yet the epigenomic and transcriptomic underpinning of vascular site-specific disease risk is largely unknown. Here, we performed single-cell chromatin accessibility (scATACseq) and gene expression profiling (scRNAseq) of mouse vascular tissue from three vascular sites. Through interrogation of epigenomic enhancers and gene regulatory networks, we discovered key regulatory enhancers to not only be cell type, but vascular site-specific.
View Article and Find Full Text PDFNat Commun
September 2025
Institute of Computational Biology, German Research Center for Environmental Health, Helmholtz Zentrum München, Neuherberg, Germany.
Atherosclerosis, a major cause of cardiovascular diseases, is characterized by the buildup of lipids and chronic inflammation in the arteries, leading to plaque formation and potential rupture. Despite recent advances in single-cell transcriptomics (scRNA-seq), the underlying immune mechanisms and transformations in structural cells driving plaque progression remain incompletely defined. Existing datasets often lack comprehensive coverage and consistent annotations, limiting the utility of downstream analyses.
View Article and Find Full Text PDFExp Gerontol
September 2025
Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA; Salk Institute for Biological Studies, La Jolla, CA, 92037, USA; Department of Molecular Biology, University of Utah, Salt Lake City, UT, USA; Department of Biochemistry, University of Utah, Salt Lake Ci
Aging is the greatest risk factor for cardiovascular diseases (CVD) and is characterized by inflammation, oxidative stress, and cellular senescence. Cellular senescence is a state of persistent cell cycle arrest triggered by stressors such as DNA damage and telomere attrition. Senescent endothelial cells (ECs) can impair vascular function and promote inflammation, thereby contributing to CVD progression.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Orthopedic Surgery, Center for Shoulder and Elbow Surgery, Konkuk University School of Medicine, Seoul, Korea.
Purpose: We aimed to compare the effects of atelocollagen (AC) and individual growth factors on the expression of key molecular markers associated with tendon healing.
Methods: C2C12 myoblasts were cultured in Dulbecco's Modified Eagle Medium (DMEM) containing 5% fetal bovine serum (FBS) and treated with 1 nM or 10 nM of Atelocollagen (AC), bone morphogenetic protein-2 (BMP-2), transforming growth factor-beta 1 (TGF-β1), insulin-like growth factor-1 (IGF-1), or vascular endothelial growth factor (VEGF) for 5 days. After 5 days of treatment, cells were harvested from the culture medium, and Western blot analysis was performed to quantify the expression of phosphorylated extracellular signal-regulated kinase (p-ERK), Collagen type I (Col I), Collagen type Ⅲ (Col Ⅲ), and Tenascin C (TnC).