Vascular smooth muscle cells (SMCs) play a key role in the development of atherosclerotic lesions. Vascular smooth muscle, however, does not represent a homogeneous tissue. Using myosin as a marker of the differentiation processes in development and in vascular disease, we have been able to demonstrate the existence of distinct SMC populations in rabbit aorta. In our studies, a specific SMC population of the aortic media showing an "immature" type of myosin isoform expression accounted for the majority of SMCs present in the atherosclerotic plaque. Nifedipine, a dihydropyridine-derived calcium antagonist, was able to decrease the size of this particular SMC population and to prevent the development of atherosclerotic lesions in hypercholesterolemic rabbits. Here we report about a similar effect obtained by treating hypercholesterolemic rabbits with nitrendipine, another dihydropyridine-derived calcium antagonist. This article also summarizes the main experimental and clinical studies conducted on the antiatherogenic effect of calcium antagonists and focuses on the mechanisms underlying this effect, particularly at the vascular SMC level.
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http://dx.doi.org/10.1097/00005344-199219002-00004 | DOI Listing |
Hypertension
January 2025
Cardiology Division, Department of Medicine, Emory University School of Medicine, Atlanta, GA. (X.Z., Q.X., A.V., Z.L.).
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Department of Radiology and Imaging Sciences, Center for Neuroimaging, Indiana University School of Medicine, Indianapolis, IN, USA.
Alzheimer's disease (AD) is a debilitating neurodegenerative disease that is marked by profound neurovascular dysfunction and significant cell-specific alterations in the brain vasculature. Recent advances in high throughput single-cell transcriptomics technology have enabled the study of the human brain vasculature at an unprecedented depth. Additionally, the understudied niche of cerebrovascular cells, such as endothelial and mural cells, and their subtypes have been scrutinized for understanding cellular and transcriptional heterogeneity in AD.
View Article and Find Full Text PDFJ Transl Med
January 2025
Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, China.
In patients with acute myocardial infarction (AMI), thrombolytic therapy and revascularization strategies allow complete recanalization of occluded epicardial coronary arteries. However, approximately 35% of patients still experience myocardial ischemia/reperfusion (I/R) injury, which contributing to increased AMI mortality. Therefore, an accurate understanding of myocardial I/R injury is important for preventing and treating AMI.
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January 2025
Center for Coronary Heart Disease, Department of Cardiology, National Center for Cardiovascular Diseases of China, State Key Laboratory of Cardiovascular Disease, Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Rd, Beijing, 100037, China.
Atherosclerosis is one of the leading causes of ischemic cardiovascular disease worldwide. Recent studies indicated that vascular smooth muscle cells (VSMCs) play an indispensable role in the progression of atherosclerosis. Exosomes derived from mesenchymal stem cells (MSCs) have demonstrated promising clinical applications in the treatment of atherosclerosis.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
January 2025
Vascular Biology Center and Department of Medicine, Medical College of Georgia at Augusta University, Augusta, GA USA.
The contribution of sex hormones to cardiovascular disease, including arterial stiffness, is established; however, the role of sex chromosome interaction with sex hormones, particularly in women, is lagging. Arterial structural stiffness depends on the intrinsic properties and transmural wall geometry that comprise a network of cells and extracellular matrix (ECM) proteins expressed in a sex-dependent manner. In this study, we used four-core genotype (FCG) mice to determine the relative contribution of sex hormones versus sex chromosomes or their interaction with arterial structural stiffness.
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