Vascular smooth muscle cells (VSMCs) constitute the principal cellular component of the medial layer of arteries and are responsible for vessel contraction and relaxation in response to blood flow. Alterations in VSMCs can hinder vascular system function, leading to vascular stiffness, calcification and atherosclerosis, which in turn may result in life-threatening complications. Pathological changes in VSMCs typically correlate with chronological age; however, there are certain conditions and diseases, such as Hutchinson-Gilford progeria syndrome (HGPS), that can accelerate this process, resulting in premature vascular aging. HGPS is a rare genetic disorder characterized by severe VSMC loss, accelerated atherosclerosis and death from myocardial infarction or stroke during the adolescence. Because experiments with mouse models have demonstrated that alterations in VSMCs are responsible for early atherosclerosis in HGPS, studies on this disease can provide insights into the mechanisms of vascular aging and assess the relative contribution of VSMCs to this process.
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http://dx.doi.org/10.1016/j.arteri.2021.11.002 | DOI Listing |
Nutrients
December 2024
Department of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou 510080, China.
Background: Atherosclerotic calcification (AC) is a common feature of atherosclerotic cardiovascular disease. β-Hydroxybutyrate (BHB) has been identified as a molecule that influences cardiovascular disease. However, whether BHB can influence AC is still unknown.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Advanced Clinical Biosystems Research Institute, Smidt Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
The prevalence of cardiovascular disease varies with sex, and the impact of intrinsic sex-based differences on vasculature is not well understood. Animal models can provide important insights into some aspects of human biology; however, not all discoveries in animal systems translate well to humans. To explore the impact of chromosomal sex on proteomic phenotypes, we used iPSC-derived vascular smooth muscle cells from healthy donors of both sexes to identify sex-based proteomic differences and their possible effects on cardiovascular pathophysiology.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Physiology, Faculty of Medicine, Semmelweis University, 37-47 Tűzoltó Street, 1094 Budapest, Hungary.
The octapeptide angiotensin II (Ang II) is a circulating hormone as well as a locally formed agonist synthesized by the angiotensin-converting enzyme (ACE) of endothelial cells. It forms a powerful mechanism to control the amount and pressure of body fluids. All main effects are directed to save body salt and water and ensure blood pressure under basic conditions and in emergencies.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Laboratory for Functional and Metabolic Imaging (LIFMET), Institute of Physics, Swiss Federal Institute of Technology (EPFL), Station 3, 1015 Lausanne, Switzerland.
Photobiomodulation (PBM) therapy, a therapeutic approach utilizing low-level light, has garnered significant attention for its potential to modulate various biological processes. This study aimed at optimizing and investigating the effects of PBM on angiogenesis and mitochondrial metabolic activity. In vitro experiments using human umbilical vein endothelial cells (HUVECs) and vascular smooth muscle cells (VSMCs) were performed to assess PBM's impacts on cell migration, proliferation, endogenous protoporphyrin IX production, mitochondrial membrane potential, Rhodamine 123 fluorescence lifetime, mitochondrial morphology, and oxygen consumption.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Institute of Physiology, University of Würzburg, 97070 Würzburg, Germany.
Nitric oxide-sensitive guanylyl cyclase (NO-GC) is a heterodimeric enzyme with an α- and a β-subunit. In its active form as an αβ-heterodimer, NO-GC produces cyclic guanosine-3',5'-monophophate (cGMP) to regulate vasodilation and proliferation of vascular smooth muscle cells (VSMCs). In contrast to VSMCs, only a few studies reported on the expression of the NO-GC αβ-heterodimer in human pericytes.
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