FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4251541073> ?p ?o ?g. }

• W4251541073 endingPage "2362" @default.
• W4251541073 startingPage "2359" @default.
• W4251541073 abstract "HomeArteriosclerosis, Thrombosis, and Vascular BiologyVol. 34, No. 11Vascular Function Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBVascular Function Hiroaki Shimokawa and Kimio Satoh Hiroaki ShimokawaHiroaki Shimokawa From the Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan. Search for more papers by this author and Kimio SatohKimio Satoh From the Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan. Search for more papers by this author Originally published21 Aug 2014https://doi.org/10.1161/ATVBAHA.114.304119Arteriosclerosis, Thrombosis, and Vascular Biology. 2014;34:2359–2362Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2014: Previous Version 1 IntroductionVascular function is regulated by many cell components, including endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and adventitial tissues with inflammatory cells, autonomic nervous system, and vasa vasorum. The interactions among these cells/tissues are substantially involved in the vascular health and disease. All these cell components secrete several growth factors, cytokines/chemokines, and extracellular matrix, all of which contribute to vascular homeostasis. Among them, the growth factors secreted from VSMCs play important roles in the vascular remodeling process because they mediate various cellular responses. In addition, oxidative stress is one of the important stimuli that modulate VSMC function and proliferation. Many recent publications in ATVB have added further information on the roles of each cell component in the regulation of vascular function and diseases, including cytokines/chemokines, matrix metalloproteinases (MMPs), VSMC proliferation, and inflammation. Some publications have also provided a novel role of perivascular adipose tissues and perivascular stem cells that contribute to the development of vascular diseases. This article will focus on these recent publications in ATVB.ECs for Vascular FunctionECs are exposed to blood flow, contributing to the maintenance of vessel structure and preservation of vascular functions. However, the effects of hemodynamic forces on cell signaling in the endothelium are still obscure. Several recent articles in ATVB addressed the role of ECs in the vascular function and mechanistic links to vascular diseases. Walshe et al1 demonstrated that transforming growth factor-β (TGF-β) signaling mediates the protective effects of shear stress on ECs. They examined the potential role of TGF-β signaling in mediating the protective effects of shear stress on ECs. Finally, they concluded that shear stress induces TGF-β3 signaling and subsequent activation of Kruppel-like factor 2 and nitric oxide (NO), demonstrating a novel role for TGF-β3 in the maintenance of endothelial homeostasis in a hemodynamic environment.1 This article provides a novel effect of shear stress on ECs in which induction of TGF-β3 expression leads to the activation of Kruppel-like factor 2 and NO signaling. Approaches designed to assess endothelial functions, as well as gene expressions in vivo, provide a novel finding in the analyses of cardiovascular diseases. As Enkhjargal et al2 have recently demonstrated, endothelial AMP-activated protein kinase mediates endothelium-dependent hyperpolarization responses and blood pressure regulation in mice. ECs are central to the initiation of vascular diseases, yet there has been limited success in studying their gene expressions in the arteries in vivo. To address this, Erbilgin et al3 developed a novel method for determining the global transcriptional changes that occur in the mouse endothelium in response to atherogenic conditions and applied it to investigate inflammatory stimuli. They demonstrated that RNA can be isolated from mouse aortic ECs after in vivo and ex vivo treatments. In addition, they applied this method to identify a group of novel causative genes in vascular diseases. Choi et al4 demonstrated that globotriaosylceramide accelerates endocytosis and lysosomal degradation of endothelial KCa3.1 via a clathrin-dependent process, leading to endothelial dysfunction in Fabry disease. In this study, the authors demonstrated that glycosphingolipid globotriaosylceramide modulates KCa3.1 expression in ECs via clathrin-dependent and early endosome antigen 1–enriched endosome-mediated lysosomal degradation. Specifically, inhibition of globotriaosylceramide –induced KCa3.1 degradation through clathrin knockdown suggested that the KCa3.1 protein is internalized by globotriaosylceramide via a clathrin-dependent process. On the basis of the study, the authors proposed a novel mechanism underlying globotriaosylceramide-mediated EC dysfunction, which is associated with suppression of endothelium-derived hyperpolarizing factors.4,5This finding is particularly important in the clinical setting. H2O2 plays a crucial role as a signaling molecule at physiological low concentrations, which is one of the endothelium-dependent hyperpolarization factors that modulate vascular tone, especially in microvessels and in human coronary arteries. Thus, physiological levels of reactive oxygen species (ROS) levels are important for the regulation of EC functions. Although high levels of ROS induce vascular dysfunction, strictly controlled ROS formation mediates several important physiological vascular functions. However, it has long been awaited a plausible explanation and mechanisms for the biphasic effect of ROS on vascular function. A recent article in ATVB by Wood et al6 demonstrated that eNOS in circulating erythrocytes also contributes to the regulation of systemic blood pressure and vascular homeostasis. Moreover, Ciccarelli et al7 demonstrated that endothelial G-protein–coupled receptor kinase 2 removal induces endothelial dysfunction by increasing endothelial ROS production. Furthermore, Zippel et al8 demonstrated that transforming growth factor-β-activated kinase 1 regulates redox balance in ECs by AMP-activated protein kinase α1, which acts as a metabolic master switch regulating several intracellular systems. In addition, Iso et al9 clearly demonstrated that capillary endothelial fatty acid–binding protein 4/5 is required for fatty acid transport into fatty acid–consuming tissues, including the heart, which controls the metabolism of energy substrates in fatty acid–consuming organs. All these recent reports focus on the crucial role of redox balance in the regulation of vascular function.Oxidative stress causes vascular dysfunction, which is closely associated with vascular inflammation. Inflammation plays a crucial role in the regulation of endothelial functions and angiogenesis. A recent article in ATVB by Wagner et al10 examined the capacity of toll-like receptor 2–blocking Abs to modulate angiogenic responses of ECs in vitro and in vivo. They identified a novel molecular mechanism linking toll-like receptor 2 to angiogenic processes that is independent from the activation of inflammatory cascades, further supporting the concept of a beneficial effect of toll-like receptor 2 inhibition for EC function in vascular disease.10 Plasma levels of high-density lipoprotein (HDL) cholesterol are inversely associated with the risk of cardiovascular diseases. Multiple lines of evidence indicate that salutary effects of HDL on ECs include antioxidative, anti-inflammatory, antithrombotic, and proangiogenic effects. A recent article in ATVB by Tatematsu et al11 reported that endothelial lipase acts on HDL to promote activation of S1P1 (sphingosine-1-phosphate receptor 1). They also showed that endothelial lipase is a key player in facilitating the activation of HDL-dependent signals that lead to S1P1 receptor activation, as well as Akt and eNOS phosphorylation.11 These results provide new insights into the molecular mechanisms through which HDL, endothelial lipase, and their interaction could modulate angiogenesis and vascular function.11VSMCs for Vascular FunctionOxidative stress plays a major role in the pathogenesis of vascular diseases. However, it remains to be elucidated which ROS promotes the development of vascular disease. A recent article in ATVB by Parastatidis et al12 examined the effect of hydrogen peroxide (H2O2)–degrading enzyme catalase on the formation of aortic aneurysms. They showed that restoration of catalase activity in the vascular wall enhances aortic VSMC survival and prevents aneurysm formation primarily through modulation of MMP activity.12 They concluded that altered H2O2 signaling as a consequence of decreased catalase activity in the vasculature could be an early insult that leads to aortic dilatation.12About the role of ROS for the development of vascular diseases, Soe et al13 also demonstrated that cyclophilin A plays a crucial role in the translocation of Nox enzymes, such as p47phox, which are known to contribute to VSMC proliferation and development of vascular diseases. Because ROS production by Nox enzymes activates other oxidase systems, cyclophilin A and Nox enzymes amplify ROS formation in a synergistic manner, leading to increased oxidative stress. Further knowledge of the role of cyclophilin A signaling on vascular cell components will contribute to the development of novel therapies for cardiovascular diseases. Rho-kinase is an important downstream effector of the small GTP-binding protein Rho and plays a crucial role in migration and proliferation of VSMCs. The RhoA/Rho-kinase pathway plays an important role in contraction, motility, and proliferation of VSMCs, leading to the development of vascular diseases. The expression of Rho-kinase is accelerated by inflammatory stimuli, which upregulates nicotinamide adenine dinucleotide phosphate oxidase and further augments ROS formation. There are 2 isoforms of Rho-kinase, ROCK1 and ROCK2, and they have different functions. However, specific roles and functional differences between ROCK1 and ROCK2 remain to be elucidated in VSMCs. In a recent issue of ATVB, Shimizu et al14 demonstrated that ROCK2 in VSMCs contributes to VSMC proliferation and pulmonary hypertension in mice and in humans. Furthermore, Ikeda et al15 demonstrated that the Rho-kinase pathway (especially ROCK2) plays a crucial role in pressure-overload–induced right ventricular hypertrophy and dysfunction. Because secretion is regulated by Rho-kinase activity, the cyclophilin A/Rho-kinase pathway contributes to augmentation of oxidative stress and the development of cardiovascular diseases.MMPs modulate extracellular matrix and regulates migration and proliferation of VSMCs. In a recent issue of ATVB, Xiao et al16 demonstrated that MMP-8 promotes VSMC proliferation and neointima formation. In this study, the authors clearly demonstrated that MMP-8 enhances VSMC proliferation via an ADAM10, N-cadherin, and β-catenin–mediated pathway and plays an important role in neointima formation. Integrins also contribute to vascular morphogenesis through regulation of adhesion and assembly of the extracellular matrix. Turlo et al17 showed an essential function of β1-integrin in the maintenance of vasomotor control and highlighted a critical role for β1-integrin in VSMC survival. Furthermore, Sutliff et al18 demonstrated that Poldip2 knockdown reduces H2O2 production in vivo, leading to increases in extracellular matrix, greater vascular stiffness, and impaired agonist-mediated contraction. Abnormal proliferation and migration of VSMCs are critical events in the progression of several vascular diseases, where AMP-activated protein kinase plays a crucial role in cellular proliferation and migration. In a recent issue of ATVB, Song et al19 demonstrated that deletion of AMP-activated protein kinase α2 causes aberrant VSMC migration with accelerated neointima formation in vivo. In the pathogenesis of pulmonary hypertension, MMP activation and VSMC proliferation/migration are substantially involved. Revuelta-López et al20 showed a crucial role of low-density lipoprotein receptor–related protein 1–mediated Pyk2 phosphorylation on hypoxia-induced MMP-9 activation, VSMC migration, and hypoxia-induced pulmonary hypertension. Low-density lipoprotein receptor–related protein 1 is a large endocytic and signaling receptor that is abundant in VSMCs. Muratoglu et al21 also suggested a critical role for low-density lipoprotein receptor–related protein 1 in maintaining the integrity of blood vessels by regulating protease activity, as well as matrix deposition by modulating HtrA1 and connective tissue growth factor. Xiao et al22 demonstrated the potential therapeutic use of the soluble Jagged1 because it not only inhibits proliferation of pulmonary VSMCs but also restores VSMCs phenotype from the dedifferentiated to the differentiated state through interference with Notch-Herp2 signaling. Finally, Dalvi et al23 showed that simultaneous exposure of pulmonary VSMCs to viral proteins and cocaine exacerbates downregulation of bone morphogenetic protein receptor. Taken together, these studies in the recent issues of ATVB have substantially contributed to the progress of our understanding on the important roles of VSMCs in the development of vascular diseases.Adventitial Tissues and Inflammatory Cells for Vascular FunctionCross talk between cells in the blood vessel wall is crucial for vascular homeostasis and diseases. EC dysfunction leads to the expression of adhesion molecules for inflammatory cells, which promotes the development of vascular diseases. The adhesion and migration of inflammatory cells produce an oxidizing environment, which is critical for the progression of vascular diseases. The accumulating inflammatory cells produce abundant ROS and secrete inflammatory cytokines and growth factors, all of which contribute to EC dysfunction and VSMC proliferation.24 In a recent issue of ATVB, Karper et al25 identified a crucial role of toll-like receptor accessory molecule RP105 on circulating inflammatory cells in atherosclerotic plaque formation. In addition, Shiomi et al26 demonstrated that coronary vasospasm could trigger coronary plaque injury and acute ischemic myocardial damage in Watanabe heritable hypercholesterolemic rabbits. Furthermore, Callegari et al27 demonstrated that osteoprotegerin derived from the bone marrow block the progression of vascular calcification.27 About the pathogenesis of aneurysms, Marinkovic et al28 performed an interesting study to limit aneurysm growth by inhibition of inflammation and reducing EC activation with immunosuppressive drug azathioprine. They showed that azathioprine has an anti-inflammatory effect in ECs and inhibits Rac1 and c-Jun-terminal-N-kinase activation, which may explain its protective role in the development of aneurysm formation and severity.28 The N-terminal lectin-like domain of thrombomodulin is known to have an anti-inflammatory function. The recent study by Lin et al29 provided a mechanism showing that recombinant thrombomodulin domain 1 can inhibit inflammation by binding to its carbohydrate ligand Le(y). However, peroxisome peroxisome proliferator-activated receptor (PPAR)-γ coactivator 1α is an important mediator of mitochondrial biogenesis and function. Because dysfunctional mitochondria are involved in the pathogenesis of vascular disease, Kröller-Schön et al30 examined the effects of peroxisome PPAR-γ coactivator 1α deficiency during chronic angiotensin II treatment in vivo. Peroxisome PPAR-γ coactivator 1α deletion caused vascular dysfunction and inflammation during chronic angiotensin II infusion by increasing mitochondrial ROS production.30 Furthermore, the findings by Doyon et al31 provided new insights into the molecular mechanism of the pathological role of angiotensin II and assist in identifying the beneficial effects of IκB kinase-β inhibition for the treatment of cardiovascular diseases. Finally, perivascular adipose tissue wraps blood vessels and modulates vasoreactivity by secretion of vasoactive molecules. Mammalian target of rapamycin complex 2 has been shown to control inflammation and is expressed in adipose tissue. Bhattacharya et al32 identified mammalian target of rapamycin complex 2 as a critical regulator of perivascular adipose tissue–directed protection of normal vascular tone. They concluded that modulation of mammalian target of rapamycin complex 2 activity in adipose tissue is a potential therapeutic approach for inflammation-related vascular damage.32SummaryIn summary, the interactions among ECs, VSMCs, adventitial tissues, and inflammatory cells regulate vascular functions and diseases. As reviewed in this highlights, recent publications in ATVB have significantly contributed to our understanding on the roles of each vascular cell component for vascular functions in health and disease. These studies have demonstrated the novel mechanistic roles of secreted factors, as well as intracellular signaling for endothelial homeostasis, VSMC proliferation, and inflammatory cell migration. Indeed, we are getting closer to the understanding of fundamental vascular functions and causative cell signaling pathways, all of which should be useful for the development of novel therapeutic strategies in cardiovascular medicine.Sources of FundingThis work was supported, in part, by the Grant-in-Aid for Tohoku University Global COE for Conquest of Signal Transduction Diseases with Network Medicine, the Grants-in-Aid for Scientific Research (21790698, 23659408, and 24390193) from the Ministry of Education, Culture, Sports, Science and Technology, Tokyo, Japan, and the Grants-in-Aid for Scientific Research (10102895) from the Ministry of Health, Labor, and Welfare, Tokyo, Japan.DisclosuresH. Shimokawa is a consultant of Asahi Kasei Pharma. K. Satoh reports no conflicts.FootnotesCorrespondence to Hiroaki Shimokawa, MD, PhD, Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai 980-8574, Japan. E-mail [email protected]References1. Walshe TE, dela Paz NG, D’Amore PA. The role of shear-induced transforming growth factor-β signaling in the endothelium.Arterioscler Thromb Vasc Biol. 2013; 33:2608–2617.LinkGoogle Scholar2. Enkhjargal B, Godo S, Sawada A, Suvd N, Saito H, Noda K, Satoh K, Shimokawa H. Endothelial AMP-activated protein kinase regulates blood pressure and coronary flow responses through hyperpolarization mechanism in mice.Arterioscler Thromb Vasc Biol. 2014; 34:1505–1513.LinkGoogle Scholar3. Erbilgin A, Siemers N, Kayne P, Yang WP, Berliner J, Lusis AJ. Gene expression analyses of mouse aortic endothelium in response to atherogenic stimuli.Arterioscler Thromb Vasc Biol. 2013; 33:2509–2517.LinkGoogle Scholar4. Choi S, Kim JA, Na HY, Cho SE, Park S, Jung SC, Suh SH. Globotriaosylceramide induces lysosomal degradation of endothelial KCa3.1 in fabry disease.Arterioscler Thromb Vasc Biol. 2014; 34:81–89.LinkGoogle Scholar5. Satoh K. Globotriaosylceramide induces endothelial dysfunction in fabry disease.Arterioscler Thromb Vasc Biol. 2014; 34:2–4.LinkGoogle Scholar6. Wood KC, Cortese-Krott MM, Kovacic JC, Noguchi A, Liu VB, Wang X, Raghavachari N, Boehm M, Kato GJ, Kelm M, Gladwin MT. Circulating blood endothelial nitric oxide synthase contributes to the regulation of systemic blood pressure and nitrite homeostasis.Arterioscler Thromb Vasc Biol. 2013; 33:1861–1871.LinkGoogle Scholar7. Ciccarelli M, Sorriento D, Franco A, Fusco A, Del Giudice C, Annunziata R, Cipolletta E, Monti MG, Dorn GW, Trimarco B, Iaccarino G. Endothelial G protein-coupled receptor kinase 2 regulates vascular homeostasis through the control of free radical oxygen species.Arterioscler Thromb Vasc Biol. 2013; 33:2415–2424.LinkGoogle Scholar8. Zippel N, Malik RA, Frömel T, Popp R, Bess E, Strilic B, Wettschureck N, Fleming I, Fisslthaler B. Transforming growth factor-β-activated kinase 1 regulates angiogenesis via AMP-activated protein kinase-α1 and redox balance in endothelial cells.Arterioscler Thromb Vasc Biol. 2013; 33:2792–2799.LinkGoogle Scholar9. Iso T, Maeda K, Hanaoka H, et al.. Capillary endothelial fatty acid binding proteins 4 and 5 play a critical role in fatty acid uptake in heart and skeletal muscle.Arterioscler Thromb Vasc Biol. 2013; 33:2549–2557.LinkGoogle Scholar10. Wagner NM, Bierhansl L, Nöldge-Schomburg G, Vollmar B, Roesner JP. Toll-like receptor 2-blocking antibodies promote angiogenesis and induce ERK1/2 and AKT signaling via CXCR4 in endothelial cells.Arterioscler Thromb Vasc Biol. 2013; 33:1943–1951.LinkGoogle Scholar11. Tatematsu S, Francis SA, Natarajan P, Rader DJ, Saghatelian A, Brown JD, Michel T, Plutzky J. Endothelial lipase is a critical determinant of high-density lipoprotein-stimulated sphingosine 1-phosphate-dependent signaling in vascular endothelium.Arterioscler Thromb Vasc Biol. 2013; 33:1788–1794.LinkGoogle Scholar12. Parastatidis I, Weiss D, Joseph G, Taylor WR. Overexpression of catalase in vascular smooth muscle cells prevents the formation of abdominal aortic aneurysms.Arterioscler Thromb Vasc Biol. 2013; 33:2389–2396.LinkGoogle Scholar13. Soe NN, Sowden M, Baskaran P, Smolock EM, Kim Y, Nigro P, Berk BC. Cyclophilin A is required for angiotensin II-induced p47phox translocation to caveolae in vascular smooth muscle cells.Arterioscler Thromb Vasc Biol. 2013; 33:2147–2153.LinkGoogle Scholar14. Shimizu T, Fukumoto Y, Tanaka S, Satoh K, Ikeda S, Shimokawa H. Crucial role of ROCK2 in vascular smooth muscle cells for hypoxia-induced pulmonary hypertension in mice.Arterioscler Thromb Vasc Biol. 2013; 33:2780–2791.LinkGoogle Scholar15. Ikeda S, Satoh K, Kikuchi N, Miyata S, Suzuki K, Omura J, Shimizu T, Kobayashi K, Kobayashi K, Fukumoto Y, Sakata Y, Shimokawa H. Crucial role of Rho-kinase in pressure overload-induced right ventricular hypertrophy and dysfunction in mice.Arterioscler Thromb Vasc Biol. 2014; 34:1260–1271.LinkGoogle Scholar16. Xiao Q, Zhang F, Grassia G, Hu Y, Zhang Z, Xing Q, Yin X, Maddaluno M, Drung B, Schmidt B, Maffia P, Ialenti A, Mayr M, Xu Q, Ye S. Matrix metalloproteinase-8 promotes vascular smooth muscle cell proliferation and neointima formation.Arterioscler Thromb Vasc Biol. 2014; 34:90–98.LinkGoogle Scholar17. Turlo KA, Scapa J, Bagher P, Jones AW, Feil R, Korthuis RJ, Segal SS, Iruela-Arispe ML. β1-integrin is essential for vasoregulation and smooth muscle survival in vivo.Arterioscler Thromb Vasc Biol. 2013; 33:2325–2335.LinkGoogle Scholar18. Sutliff RL, Hilenski LL, Amanso AM, Parastatidis I, Dikalova AE, Hansen L, Datla SR, Long JS, El-Ali AM, Joseph G, Gleason RL, Taylor WR, Hart CM, Griendling KK, Lassègue B. Polymerase delta interacting protein 2 sustains vascular structure and function.Arterioscler Thromb Vasc Biol. 2013; 33:2154–2161.LinkGoogle Scholar19. Song P, Zhou Y, Coughlan KA, Dai X, Xu H, Viollet B, Zou MH. Adenosine monophosphate-activated protein kinase-α2 deficiency promotes vascular smooth muscle cell migration via S-phase kinase-associated protein 2 upregulation and E-cadherin downregulation.Arterioscler Thromb Vasc Biol. 2013; 33:2800–2809.LinkGoogle Scholar20. Revuelta-López E, Castellano J, Roura S, Gálvez-Montón C, Nasarre L, Benitez S, Bayes-Genis A, Badimon L, Llorente-Cortés V. Hypoxia induces metalloproteinase-9 activation and human vascular smooth muscle cell migration through low-density lipoprotein receptor-related protein 1-mediated Pyk2 phosphorylation.Arterioscler Thromb Vasc Biol. 2013; 33:2877–2887.LinkGoogle Scholar21. Muratoglu SC, Belgrave S, Hampton B, Migliorini M, Coksaygan T, Chen L, Mikhailenko I, Strickland DK. LRP1 protects the vasculature by regulating levels of connective tissue growth factor and HtrA1.Arterioscler Thromb Vasc Biol. 2013; 33:2137–2146.LinkGoogle Scholar22. Xiao Y, Gong D, Wang W. Soluble JAGGED1 inhibits pulmonary hypertension by attenuating notch signaling.Arterioscler Thromb Vasc Biol. 2013; 33:2733–2739.LinkGoogle Scholar23. Dalvi P, O’Brien-Ladner A, Dhillon NK. Downregulation of bone morphogenetic protein receptor axis during HIV-1 and cocaine-mediated pulmonary smooth muscle hyperplasia: implications for HIV-related pulmonary arterial hypertension.Arterioscler Thromb Vasc Biol. 2013; 33:2585–2595.LinkGoogle Scholar24. Tedgui A, Ait-Oufella H. Innate lymphoid cells: new players in atherosclerosis?Arterioscler Thromb Vasc Biol. 2013; 33:2697–2698.LinkGoogle Scholar25. Karper JC, de Jager SC, Ewing MM, de Vries MR, Bot I, van Santbrink PJ, Redeker A, Mallat Z, Binder CJ, Arens R, Jukema JW, Kuiper J, Quax PH. An unexpected intriguing effect of Toll-like receptor regulator RP105 (CD180) on atherosclerosis formation with alterations on B-cell activation.Arterioscler Thromb Vasc Biol. 2013; 33:2810–2817.LinkGoogle Scholar26. Shiomi M, Ishida T, Kobayashi T, Nitta N, Sonoda A, Yamada S, Koike T, Kuniyoshi N, Murata K, Hirata K, Ito T, Libby P. Vasospasm of atherosclerotic coronary arteries precipitates acute ischemic myocardial damage in myocardial infarction-prone strain of the Watanabe heritable hyperlipidemic rabbits.Arterioscler Thromb Vasc Biol. 2013; 33:2518–2523.LinkGoogle Scholar27. Callegari A, Coons ML, Ricks JL, Yang HL, Gross TS, Huber P, Rosenfeld ME, Scatena M. Bone marrow- or vessel wall-derived osteoprotegerin is sufficient to reduce atherosclerotic lesion size and vascular calcification.Arterioscler Thromb Vasc Biol. 2013; 33:2491–2500.LinkGoogle Scholar28. Marinkovic G, Hibender S, Hoogenboezem M, van Broekhoven A, Girigorie AF, Bleeker N, Hamers AA, Stap J, van Buul JD, de Vries CJ, de Waard V. Immunosuppressive drug azathioprine reduces aneurysm progression through inhibition of Rac1 and c-Jun-terminal-N-kinase in endothelial cells.Arterioscler Thromb Vasc Biol. 2013; 33:2380–2388.LinkGoogle Scholar29. Lin WL, Chang CF, Shi CS, Shi GY, Wu HL. Recombinant lectin-like domain of thrombomodulin suppresses vascular inflammation by reducing leukocyte recruitment via interacting with Lewis Y on endothelial cells.Arterioscler Thromb Vasc Biol. 2013; 33:2366–2373.LinkGoogle Scholar30. Kröller-Schön S, Jansen T, Schüler A, Oelze M, Wenzel P, Hausding M, Kerahrodi JG, Beisele M, Lackner KJ, Daiber A, Münzel T, Schulz E. Peroxisome proliferator-activated receptor γ, coactivator 1α deletion induces angiotensin II-associated vascular dysfunction by increasing mitochondrial oxidative stress and vascular inflammation.Arterioscler Thromb Vasc Biol. 2013; 33:1928–1935.LinkGoogle Scholar31. Doyon P, van Zuylen WJ, Servant MJ. Role of IκB kinase-β in the growth-promoting effects of angiotensin II in vitro and in vivo.Arterioscler Thromb Vasc Biol. 2013; 33:2850–2857.LinkGoogle Scholar32. Bhattacharya I, Drägert K, Albert V, Contassot E, Damjanovic M, Hagiwara A, Zimmerli L, Humar R, Hall MN, Battegay EJ, Haas E. Rictor in perivascular adipose tissue controls vascular function by regulating inflammatory molecule expression.Arterioscler Thromb Vasc Biol. 2013; 33:2105–2111.LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Nevado R, Hamczyk M and Andrés V (2022) Isolation of Mouse Aortic RNA for Transcriptomics Atherosclerosis, 10.1007/978-1-0716-1924-7_38, (611-627), . Emamat H, Mousavi S, Kargar Shouraki J, Hazrati E, Mirghazanfari S, Samizadeh E, Hosseini M, Hadi V and Hadi S (2022) The effect of Nigella sativa oil on vascular dysfunction assessed by flow‐mediated dilation and vascular‐related biomarkers in subject with cardiovascular disease risk factors: A randomized controlled trial , Phytotherapy Research, 10.1002/ptr.7441, 36:5, (2236-2245), Online publication date: 1-May-2022. Satoh K and Shimokawa H (2021) Pathophysiology and Molecular Mechanisms of Coronary Artery Spasm Coronary Vasomotion Abnormalities, 10.1007/978-981-15-7594-5_2, (21-37), . He Z, Wang G, Wu J, Tang Z and Luo M (2021) The molecular mechanism of LRP1 in physiological vascular homeostasis and signal transduction pathways, Biomedicine & Pharmacotherapy, 10.1016/j.biopha.2021.111667, 139, (111667), Online publication date: 1-Jul-2021. Satoh K (2021) Drug discovery focused on novel pathogenic proteins for pulmonary arterial hypertension, Journal of Cardiology, 10.1016/j.jjcc.2021.01.009, 78:1, (1-11), Online publication date: 1-Jul-2021. Marques B, Klein M, da Cunha M, de Souza Mattos S, de Paula Nogueira L, de Paula T, Corrêa F, Oigman W and Neves M (2019) Effects of Oral Magnesium Supplementation on Vascular Function: A Systematic Review and Meta-analysis of Randomized Controlled Trials, High Blood Pressure & Cardiovascular Prevention, 10.1007/s40292-019-00355-z, 27:1, (19-28), Online publication date: 1-Feb-2020. Amadi P, Agomuo E and Adumekwe C (2020) Modulatory properties of cardiac and quercetin glycosides from Dacryodes edulis seeds during L-NAME-induced vascular perturbation , Journal of Basic and Clinical Physiology and Pharmacology, 10.1515/jbcpp-2019-0116, 31:5, Online publication date: 26-Aug-2020., Online publication date: 1-Sep-2020. Satoh K, Satoh T, Yaoita N and Shimokawa H (2019) Recent Advances in the Understanding of Thrombosis, Arteriosclerosis, Thrombosis, and Vascular Biology, 39:6, (e159-e165), Online publication date: 1-Jun-2019. Dou F, Wu B, Sun L, Chen J, Liu T, Yu Z and Chen C (2019) Identification of a novel regulatory pathway for PPARα by RNA-seq characterization of the endothelial cell lipid peroxidative injury transcriptome, Open Biology, 10.1098/rsob.190141, 9:12, (190141), Online publication date: 1-Dec-2019. Satoh K and Shimokawa H (2018) Recent Advances in the Development of Cardiovascular Biomarkers, Arteriosclerosis, Thrombosis, and Vascular Biology, 38:5, (e61-e70), Online publication date: 1-May-2018.Godo S and Shimokawa H (2017) Endothelial Functions, Arteriosclerosis, Thrombosis, and Vascular Biology, 37:9, (e108-e114), Online publication date: 1-Sep-2017. Satoh K (2017) Development of Novel Therapies for Cardiovascular Diseases by Clinical Application of Basic Research, Circulation Journal, 10.1253/circj.CJ-17-1029, 81:11, (1557-1563), . Karimi Galougahi K, Ashley E and Ali Z (2015) Redox regulation of vascular remodeling, Cellular and Molecular Life Sciences, 10.1007/s00018-015-2068-y, 73:2, (349-363), Online publication date: 1-Jan-2016. Romero M, Yahagi K, Kolodgie F and Virmani R (2015) Neoatherosclerosis From a Pathologist’s Point of View, Arteriosclerosis, Thrombosis, and Vascular Biology, 35:10, (e43-e49), Online publication date: 1-Oct-2015. Satoh K (2015) Cyclophilin A in Cardiovascular Homeostasis and Diseases, The Tohoku Journal of Experimental Medicine, 10.1620/tjem.235.1, 235:1, (1-15), . Wang T, Chang M, Li Y, Huang T, Chien S and Wu C (2021) Maintenance of HDACs and H3K9me3 Prevents Arterial Flow-Induced Venous Endothelial Damage, Frontiers in Cell and Developmental Biology, 10.3389/fcell.2021.642150, 9 Rodríguez-Rodríguez R, Ackermann T, Plaza J, Simonsen U, Matchkov V, Llobera A and Munoz-Berbel X (2019) Ultrasensitive Photonic Microsystem Enabling Sub-micrometric Monitoring of Arterial Oscillations for Advanced Cardiovascular Studies, Frontiers in Physiology, 10.3389/fphys.2019.00940, 10 Locatelli L, Castiglioni S and Maier J (2022) From Cultured Vascular Cells to Vessels: The Cellular and Molecular Basis of Vascular Dysfunction in Space, Frontiers in Bioengineering and Biotechnology, 10.3389/fbioe.2022.862059, 10 November 2014Vol 34, Issue 11 Advertisement Article InformationMetrics © 2014 American Heart Association, Inc.https://doi.org/10.1161/ATVBAHA.114.304119PMID: 25147337 Originally publishedAugust 21, 2014 Keywordsmuscle, smooth, vascularendothelial cellsPDF download Advertisement SubjectsEndothelium/Vascular Type/Nitric OxideMechanismsSmooth Muscle Proliferation and Differentiation" @default.
• W4251541073 created "2022-05-12" @default.
• W4251541073 creator A5012657143 @default.
• W4251541073 creator A5087369181 @default.
• W4251541073 date "2014-11-01" @default.
• W4251541073 modified "2023-10-18" @default.
• W4251541073 title "Vascular Function" @default.
• W4251541073 cites W1963972436 @default.
• W4251541073 cites W1985396890 @default.
• W4251541073 cites W2002155793 @default.
• W4251541073 cites W2036409505 @default.
• W4251541073 cites W2050013520 @default.
• W4251541073 cites W2096498029 @default.
• W4251541073 cites W2099073051 @default.
• W4251541073 cites W2105240342 @default.
• W4251541073 cites W2105609828 @default.
• W4251541073 cites W2106397291 @default.
• W4251541073 cites W2113278438 @default.
• W4251541073 cites W2118265634 @default.
• W4251541073 cites W2123675100 @default.
• W4251541073 cites W2124913297 @default.
• W4251541073 cites W2127777722 @default.
• W4251541073 cites W2131290609 @default.
• W4251541073 cites W2140121390 @default.
• W4251541073 cites W2140453450 @default.
• W4251541073 cites W2145082590 @default.
• W4251541073 cites W2145507715 @default.
• W4251541073 cites W2145676650 @default.
• W4251541073 cites W2147049940 @default.
• W4251541073 cites W2147881867 @default.
• W4251541073 cites W2153065274 @default.
• W4251541073 cites W2154455571 @default.
• W4251541073 cites W2155844903 @default.
• W4251541073 cites W2156369702 @default.
• W4251541073 cites W2161122421 @default.
• W4251541073 cites W2163490310 @default.
• W4251541073 cites W2164483611 @default.
• W4251541073 cites W2169143571 @default.
• W4251541073 cites W2170525200 @default.
• W4251541073 doi "https://doi.org/10.1161/atvbaha.114.304119" @default.
• W4251541073 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25147337" @default.
• W4251541073 hasPublicationYear "2014" @default.
• W4251541073 type Work @default.
• W4251541073 citedByCount "22" @default.
• W4251541073 countsByYear W42515410732015 @default.
• W4251541073 countsByYear W42515410732017 @default.
• W4251541073 countsByYear W42515410732018 @default.
• W4251541073 countsByYear W42515410732019 @default.
• W4251541073 countsByYear W42515410732020 @default.
• W4251541073 countsByYear W42515410732021 @default.
• W4251541073 countsByYear W42515410732022 @default.
• W4251541073 countsByYear W42515410732023 @default.
• W4251541073 crossrefType "journal-article" @default.
• W4251541073 hasAuthorship W4251541073A5012657143 @default.
• W4251541073 hasAuthorship W4251541073A5087369181 @default.
• W4251541073 hasBestOaLocation W42515410731 @default.
• W4251541073 hasConcept C14036430 @default.
• W4251541073 hasConcept C78458016 @default.
• W4251541073 hasConcept C86803240 @default.
• W4251541073 hasConceptScore W4251541073C14036430 @default.
• W4251541073 hasConceptScore W4251541073C78458016 @default.
• W4251541073 hasConceptScore W4251541073C86803240 @default.
• W4251541073 hasIssue "11" @default.
• W4251541073 hasLocation W42515410731 @default.
• W4251541073 hasLocation W42515410732 @default.
• W4251541073 hasOpenAccess W4251541073 @default.
• W4251541073 hasPrimaryLocation W42515410731 @default.
• W4251541073 hasRelatedWork W2355042795 @default.
• W4251541073 hasRelatedWork W2355200970 @default.
• W4251541073 hasRelatedWork W2364631038 @default.
• W4251541073 hasRelatedWork W2365846570 @default.
• W4251541073 hasRelatedWork W2368137809 @default.
• W4251541073 hasRelatedWork W2375986632 @default.
• W4251541073 hasRelatedWork W2376525345 @default.
• W4251541073 hasRelatedWork W2386751173 @default.
• W4251541073 hasRelatedWork W2389790749 @default.
• W4251541073 hasRelatedWork W2392519414 @default.
• W4251541073 hasVolume "34" @default.
• W4251541073 isParatext "false" @default.
• W4251541073 isRetracted "false" @default.
• W4251541073 workType "article" @default.