Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/jdv.15864 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
CCAAT/Enhancer-Binding Protein β (C/EBPβ) Regulates Calcium Deposition in Smooth Muscle Cells.
Int J Mol Sci
December 2024
Department of Pharmacology, Chonnam National University Medical School, Hwasun 58128, Republic of Korea.
Calcium deposition in vascular smooth muscle cells (VSMCs), a form of ectopic ossification in blood vessels, can result in rigidity of the vasculature and an increase in cardiac events. Here, we report that CCAAT/enhancer-binding protein beta (C/EBPβ) potentiates calcium deposition in VSMCs and mouse aorta induced by inorganic phosphate (Pi) or vitamin D. Based on cDNA microarray and RNA sequencing data of Pi-treated rat VSMCs, C/EBPβ was found to be upregulated and thus selected for further evaluation.
View Article and Find Full Text PDFNative Valve and Native Neo-Sinus Remodeling Following Transcatheter Aortic Valve Replacement.
Circ Cardiovasc Interv
December 2024
Cardiovascular Translational Laboratory, Providence Research and Centre for Heart Lung Innovation, Vancouver, British Columbia, Canada (J.Y., H.G., J.J., A.L., J.G.W., J.S., D.M., S.L.S.).
Background: Transcatheter aortic valve replacement (TAVR) pushes aside the diseased native aortic valve and creates a native neo-sinus bordered by the aortic root wall and the displaced native valve. There are limited data on the progression of native valve disease post-TAVR and no previous analysis of the native neo-sinus.
Methods: Native aortic valves and native neo-sinus explants obtained post-TAVR were evaluated histologically (hematoxylin and eosin, Movat pentachrome, and Martius Scarlet Blue stains) and by immunohistochemistry (TGF-β1 [transforming growth factor-beta 1], FAP [fibroblast activation protein], and ALP [alkaline phosphatase]) to assess disease mechanisms.
Severe Coronary Artery Calcifications in Chronic Kidney Disease Patients, Coupled with Inflammation and Bone Mineral Disease Derangement, Promote Major Adverse Cardiovascular Events through Vascular Remodeling.
Kidney Blood Press Res
January 2025
PhyMedExp, University of Montpellier, INSERM, CNRS, Department of Biochemistry and Hormonology, University Hospital Center of Montpellier, Montpellier, France.
Article Synopsis
- Cardiovascular diseases are the leading cause of illness and death in chronic kidney disease patients, with a study analyzing the impact of coronary artery calcifications (CAC) and cardiovascular biomarkers on major adverse cardiovascular events and deaths.
- The study involved 425 non-dialysis CKD patients who underwent scans for CAC scoring and measurement of various cardiovascular risk biomarkers, with follow-up lasting an average of about 3.6 years.
- Findings indicate that high CAC levels significantly increase the risk of major adverse cardiovascular events, especially when combined with certain inflammatory and metabolic conditions, suggesting that managing inflammation and improving mineral metabolism could be key strategies for reducing cardiovascular risk in these patients.
Matrix vesicles from osteoblasts promote atherosclerotic calcification.
Matrix Biol
December 2024
Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, PR China. Electronic address:
Atherosclerotic calcification often coincides with osteoporosis, suggesting a potential interplay between bone and vascular mineralization. Osteoblast-derived matrix vesicles (Ost-MVs), pivotal in bone mineralization, have emerged as potential contributors to ectopic vascular calcification. However, the precise role of Ost-MVs in vascular calcification and the underlying mechanisms remain elusive.
View Article and Find Full Text PDFRUNX2 is stabilised by TAZ and drives pulmonary artery calcification and lung vascular remodelling in pulmonary hypertension due to left heart disease.
Eur Respir J
November 2024
Institute for Physiology, Charité - Universitätsmedizin Berlin, corporate member of the Free University Berlin and the Humboldt University Berlin, Berlin, Germany.
Article Synopsis
- Calcification in pulmonary hypertension associated with left heart disease appears to be influenced by the interaction between RUNX2 and TAZ, which are key regulators in osteogenic processes.
- Significant vascular calcification was observed in both patients and rat models, with elevated levels of RUNX2 and TAZ.
- Inhibiting TAZ or RUNX2 effectively reduced vascular calcification and the progression of pulmonary hypertension in the rat model, suggesting potential therapeutic targets.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!