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TWEAK/Fn14 axis may promote vascular smooth muscle cell senescence via p38 signaling pathway: preliminary evidence.
Future Sci OA
December 2025
Department of Gerontology, the First Affiliated Hospital, China Medical University, Shenyang, China.
Aim: The primary objective of this study is to investigate the impact of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), on the process of vascular smooth muscle cell (VSMC) senescence.
Methods: Rat arterial VSMCs were cultured with angiotensin II to establish a model of premature senescence. The effects of TWEAK and Fn14 on senescent VSMCs were evaluated.
The Correlation of Serum Adropin with Cardiovascular Risk Factors in the Experimental Rat Model of Chronic Kidney Disease and Its Implication in the Ameliorative Effect of Angiotensin-Converting Enzyme Inhibitors.
Iran J Med Sci
December 2024
Department of Medical Physiology, College of Medicine, Zagazig University, Al-Sharquia, Egypt.
Background: The risk of cardiovascular disease (CVD) in patients with chronic kidney disease (CKD) is estimated to be far greater than that in the general population. Adropin regulates endothelial function and may play a role in the pathogenesis of CVD. Angiotensin-converting enzyme inhibitor (ACEI) treatment was reported to have a protective effect on both renal and cardiovascular function.
View Article and Find Full Text PDFUpregulation of Piezo2 and increased extracellular matrix protein in diabetic kidney disease mice.
Hypertens Res
January 2025
Department of Anatomy, Kyorin University School of Medicine, Mitaka, Tokyo, Japan.
Mechanical forces such as glomerular hyperfiltration are crucial in the pathogenesis and progression of diabetic kidney disease. Piezo2 is a mechanosensitive cation channel and plays a major role in various biological and pathophysiological phenomena. We previously reported Piezo2 expression in mouse and rat kidneys and its alteration by dehydration and hypertension.
View Article and Find Full Text PDFJOSD2 inhibits angiotensin II-induced vascular remodeling by deubiquitinating and stabilizing SMAD7.
Acta Pharmacol Sin
January 2025
Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, China.
Increased level of angiotensin II (Ang II) plays a central role in the development of hypertensive vascular remodeling. In this study, we identified the deubiquitinating enzyme Josephin domain-containing protein 2 (JOSD2) as a protective factor and investigated its molecular mechanism in Ang II-induced vascular remodeling. First, we found that JOSD2 was upregulated in aortic smooth muscle cells, but not in endothelial cells of Ang II-challenged mouse vascular tissues.
View Article and Find Full Text PDFAnalysis of cellular NO-GC expression in the murine heart and lineage determination in angiotensin II-induced fibrosis.
iScience
January 2025
Physiologisches Institut, Julius-Maximilians-Universität Würzburg, Würzburg, Germany.
NO-sensitive guanylyl cyclase (NO-GC) is involved in the (patho)physiology of the mammalian heart. However, little is known about the individual cardiac cell types that express NO-GC and the role of the enzyme in cardiac fibrosis. Here, we describe the cellular expression of NO-GC in healthy and fibrotic murine myocardium; these data were compared with scRNA-seq data.
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