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Structural Cardiovascular Changes in Hypertension
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
M. Mulvany, Enrico Agabiti Rosei, H. Struijker-Boudier
Another genetic approach, particularly followed by Lacolley, Laurent and their co-workers, is the study of large artery properties in subjects with monogenic disease or in knockout mice with phenotype changes in arterial wall properties (25,27). The data obtained following this approach highlight the role of vascular smooth muscle cells and extracellular matrix components. Furthermore, the data show that collagen and elastin are not simply passive compounds that can be elastic or rigid, but that they are also involved in the control of VSMC function, such as migration, proliferation, adhesion and cytoskeletal rearrangement (25,27) and may thus influence large artery properties in different ways.
Vascular Smooth Muscle Cells
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
Lars M. Rasmussen, Jens L. Andresen, Thomas Ledet
Arterial smooth muscle cells are responsible for maintaining both arterial tension by contraction-relaxation and blood-vessel integrity by proliferation, migration, and synthesis of extracellular matrix. In a normal blood vessel, smooth muscle cells respond by contraction or relaxation to blood pressure-regulating factors derived from the blood or produced locally in overlaying endothelial cells, thereby determining the tone of the vessel.79 Vascular smooth muscle cells do, however, play other roles than merely being responder cells determining vascular tone; proliferative, migrative and synthetic properties of these cells are key functions during the development of blood vessels and in the maintenance of normal vessel integrity, but also in many pathological situations. Thus, accumulation of vascular smooth muscle cells and their matrix is one hallmark of fibrous atherosclerotic plaques99 and restenotic lesions after arterial injury.30,84,118 In addition, hypertension is associated with structural alterations in the wall of small arteries.9,41 In diabetic angiopathy, vascular smooth muscle cells in both small and large vessels seem to be involved, since altered biochemical composition and structural properties of the extracellular matrix has been reported.61,94,95
Inhibiting Low-Density Lipoproteins Intimal Deposition and Preserving Nitric Oxide Function in the Vascular System
Published in Christophe Wiart, Medicinal Plants in Asia for Metabolic Syndrome, 2017
Methanolic extract of tubers of Corydalis turtschaninovii Besser inhibited the enzymatic activity of aldose reductase.90 From the same tubers, glaucine, protopine, and dehydrocorynaline inhibited the enzymatic activity of aldose reductase by 16.5%, 10.9%, and 44.5% at a dose of 50 µM.90 Tetrahydropalmatine given at a single dose of 10 mg/kg intravenously to anesthetized rodents evoked an immediate and transient fall of mean arterial blood pressure (by 38 mmHg), a reduction of heart rate (by 43 beats/min), and a decrease in hypothalamic serotonine release (by 52%).91 The hypotension and bradycardia evoked by tetrahydropalmatine were inhibited by the 5-HT2 receptor agonist DOI.91 Furthermore, spinal section and bilateral vagotomy attenuated tetrahydropalmatine-induced hypotension and bradycardia, respectively.91 Arachidonic from cytoplasmic membrane phospholipids of platelets is converted to thromboxane A2 under the combined action of cyclo-oxygenase and thromboxane A2 synthetase.92 The plant contains tetrahydroberberine, which inhibited the aggregation of platelets challenged with arachidonic acid, adenosine diphosphate, and collagen.93 Besides, tetrahydroberberine inhibited the generation of thromboxane B2 in platelets exposed to arachidonic acid.93 Tetrahydroberberine at a dose of 30 mg/kg/day given intraperitoneally for 5 days negated the aggregation of platelets induced by ADP in rodents.93 Sanguinarine (Figure 5.7) inhibited the aggregation of platelets evoked by arachidonic acid and collagen with IC50 values equal to 8.3 µM and 7.7 mM.94 Against thrombin, sanguinarine inhibited platelet aggregation by 10% at a concentration of 10 µM.94 Sanguinarine inhibited the aggregation of platelets induced by the thromboxane A2 analog U46619 with an IC50 of 8.6 µM.94 The adenylate cyclase inhibitor SQ22536 attenuated the inhibitory effect of sanguinarine against the platelet aggregation evoked by arachidonic acid.94 Sanguinarine inhibited the production of thromboxane B2 by platelets challenged with arachidonic acid with an IC50 of 4.5 µM and inhibited the enzymatic activity of cyclooxygenase-1 with an IC50 value of 28 µM.94 This alkaloid at 300 nM inhibited the multiplication of vascular smooth muscle cells by arresting cell cycle in G1 with induction of p27, decrease in the enzymatic activities of CDK2 and CDK4, and induction of Ras and extracellular signal-regulated kinase-1/2.95 Chelerythrine at 8 µmol/L prevented hypertrophy of neonatal ventricular myocytes of rodents exposed to high glucose levels via reduction of protein kinase Cα (PKC-α) and protein kinase β2 (PKC- β2).96 The control of growth of vascular smooth muscle cells has critical therapeutic implication for atherosclerosis.97
Association of Circular RNAs levels in blood and Essential Hypertension with Carotid Plaque
Published in Clinical and Experimental Hypertension, 2023
Haiyan Qian, Zebo Zhang, Zhenbo Tao, Yanqing Xie, Yueqi Yin, Wenming He, Lina Zhang
Circular RNAs (circRNAs) are covalently closed cyclic molecules without 5ʹor 3ʹ ends, which can be divided into non-coding circRNAs and coding circRNAs according to whether they can be translated (10). Some circRNAs are rich in miRNA response elements and act as “miRNA sponges” to competitively bind to miRNAs, thereby regulating the expression of miRNA target genes, the so-called competing endogenous RNA (ceRNA) (11). In recent years, several studies have shown that circRNAs are related to the molecular mechanism of endothelial dysfunction which is strongly associated with hypertension and atherosclerosis (12–14). In addition, the aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) trigger a key step in the pathogenesis of atherosclerosis. CircCHFR facilitates the proliferation and migration of VSMCs via miR-370/FOXO1/Cyclin D1 pathway, while circMap3k5, a sponge of miR-22-3p, hinders proliferation and promotes differentiation of VSMCs (15,16). However, the role of circRNAs in hypertensive patients with carotid atherosclerosis remains unclear.
Methylglyoxal stimulates endoplasmic reticulum stress in vascular smooth muscle cells
Published in Journal of Receptors and Signal Transduction, 2022
Vascular smooth muscle cells (VSMCs) play a prominent role in atherosclerosis. These cells actively contribute to plaque structure by displaying elevated proliferation and migration in plaque progression steps. In contrast, apoptosis of VSMCs in advanced atherosclerotic plaques causes the plaque’s rupture and may cause a stroke. Briefly, at the early steps of atherosclerosis, abnormal proliferation and migration of VSMCs are not desired. Besides, their apoptosis is not preferred at advanced plaques as they stabilize the plaque [10]. There is limited study in the literature focusing on ER stress in VSMCs. ER stress inducer tunicamycin protected VSMCs from PDGF-BB-induced activation [11]. 7-Ketocholesterol (rich in atherosclerotic plaques) stimulated ER stress in VSMCs and activated cells’ apoptosis [12]. Hyperhomocysteinemia [13] and glucosamine induced ER stress in VSMCs and contributed to accelerated atherosclerosis pathology [14]. In this study, we inspected whether MGO induces ER stress in VSMCs. ER stress signaling pathways PERK phosphorylation, IRE1α, ATF6, Bip (Grp78), and CHOP expressions were studied for this aim. Also, MGO-induced apoptosis of the cells was explored. Aminoguanidine hydrochloride (AGH), 4-phenylbutyric acid (4-PBA), and tauroursodeoxycholic acid (TUDCA) were evaluated to alleviate MGO-induced ER stress.
Drug-eluting stents for the treatment of coronary artery disease: A review of recent advances
Published in Expert Opinion on Drug Delivery, 2022
As for drugs, mTOR inhibitors, such as sirolimus and its analog are very effective in preventing restenosis. However, traditional mTOR inhibitors are also known to be associated with endothelial barrier dysfunction which might have an important role in the pathogenesis of neoatherosclerosis after DES implantation. A next-generation selective’ mTOR kinase inhibitor that does not bind to FKBP12 but inhibits mTOR directly, endothelial barrier function theoretically can be preserved while inhibiting neointimal formation. In addition, though the currently used drugs have been mostly targeted to inhibit vascular smooth muscle cell proliferation to reduce intimal proliferation, drugs with several actions might be used for different purposes or as combination therapy to reduce inflammation, platelet activation, or thrombosis.