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Published: 10 December 2022
Last updated: 29 January 2023

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1

Schrör, Karsten, and Peter Ney, eds. Prostaglandins and Control of Vascular Smooth Muscle Cell Proliferation. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-7352-9.

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2

Hamel, Kenneth Carl. The role of activin in aortic smooth muscle cell growth. Ottawa: National Library of Canada, 1993.

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3

Leung, Wesley D. The role of apolipoprotein D in vascular smooth muscle cell migration. Ottawa: National Library of Canada, 2002.

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4

Sarjeant, Jennifer Mary. The role of apolipoprotein D in vascular smooth muscle cell proliferation. Ottawa: National Library of Canada, 2002.

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5

Mitchell, Lylieth Paula-Ann. Vascular endothelial and smooth muscle cell apoptosis in vivo and in vitro. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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6

rdh-Nilsson, Anna Hultga. Oncogenes and second messengers in the regulation of smooth muscle cell growth and differentiation. Stockholm: Kongl. Carolinska Medico Chirurgiska Institutet, 1991.

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7

Hultgardh-Nilsson, Anna. Oncogenes and second messengers in the regulation of smooth muscle cell growth and differentiation. [S.l: s.n.], 1991.

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8

D, Huizinga Jan, ed. Pacemaker activity and intercellular communication. Boca Raton: CRC Press, 1995.

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9

Ho, Bernard. Integrin-linked kinase in the vascular smooth muscle cell response to arterial injury. 2006.

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10

Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.

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Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of non-immune cells such as platelets, endothelial, and vascular smooth muscle cells, in its pathogenesis. This chapter highlights the roles of these individual cell types in atherogenesis and explains their modes of communication using chemokines, cytokines, and co-stimulatory molecules.
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11

Disclosure of novel mechanisms in which nicotine triggers structural and functional alterations of arterial smooth muscle cells: Implications to pathogenesis of the occlusive arterial diseases. Ottawa: National Library of Canada, 2001.

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12

Positive remodeling in venous bypass grafts & the phenotypic differences between venous and arterial smooth muscle cells: Novel implications toward vein graft failure. Ottawa: National Library of Canada, 2003.

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13

Bodnaruk, Tetyana Daria Evhenia. Neuraminidase-1, a subunit of the elastin receptor, alters mitogenic growth factor receptors and down-regulates proliferation of arterial smooth muscle cells. 2006.

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14

Bochaton-Piallat, Marie-Luce, Carlie J. M. de Vries, and Guillaume J. van Eys. Vascular smooth muscle cells. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0007.

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To understand the function of arteries in the regulation of blood supply throughout the body it is essential to realize that the vessel wall is composed predominantly of smooth muscle cells (SMCs) with only one single layer of luminal endothelial cells. SMCs determine the structure of arteries and are decisive in the regulation of blood flow. This review describes the reason for the large variation of SMCs throughout the vascular tree. This depends on embryonic origin and local conditions. SMCs have the unique capacity to react to these conditions by modulating their phenotype. So, in one situation SMCs may be contractile in response to blood pressure, in another situation they may be synthetic, providing compounds to increase the strength of the vascular wall by reinforcing the extracellular matrix. This phenotypic plasticity is necessary to keep arteries functional in fulfilling the metabolic demands in the various tissues of the body.
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15

The Vascular Smooth Muscle Cell. Elsevier, 1995. http://dx.doi.org/10.1016/b978-0-12-632310-8.x5000-1.

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16

Karsten, Schrör, and Ney Peter 1930-, eds. Prostaglandins and control of vascular smooth muscle cell proliferation. Basel, Switzerland ; Boston, Mass: Birkhäuser Verlag, 1997.

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17

Nev, P., and K. Schrör. Prostaglandins and Control of Vascular Smooth Muscle Cell Proliferation. Springer Basel AG, 2012.

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18

Liu, Tianbiao. IGF-1 transfection enhances cardiac smooth muscle cell engraftment. 2004.

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19

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.
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20

Schwartz, Stephen M., and Robert P. Mecham. Vascular Smooth Muscle Cell: Molecular and Biological Responses to the Extracellular Matrix. Elsevier Science & Technology Books, 1995.

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21

M, Schwartz Stephen, and Mecham Robert P, eds. The vascular smooth muscle cell: Molecular and biological responses to the extracellular matrix. San Diego: Academic Press, 1995.

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22

The Vascular Smooth Muscle Cell: Molecular and Biological Responses to the Extracellular Matrix (Biology of Extracellular Matrix). Academic Press, 1995.

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23

Schwartz, Stephen M. The Vascular Smooth Muscle Cell: Molecular and Biological Responses to the Extracellular Matrix (Biology of Extracellular Matrix). Academic Press, 1995.

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24

Sci, International Union Of Physiological. Regulation and Contraction of Smooth Muscle: Proceedings of an International Union on Physiological Sciences Satellite Conference on Smooth Muscle Con (Modern Cell Biology). Alan R. Liss, 1987.

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25

Song, Ping, Xiaoyan Dai, Qilong Wang, and Vicky E. MacRae, eds. Vascular Smooth Muscle Cell fate and Vascular Remodeling: Mechanisms, Therapeutic Targets, and Drugs, Volume I. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-070-5.

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26

Liu, Elsa Hin-Yee. The effects of doxycycline regulation on fibrillar collagen production in long term smooth muscle cell culture. 2004.

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27

1946-, Bruschi G., and Borghetti Alberico, eds. Cellular aspects of hypertension. Berlin: Springer-Verlag, 1991.

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28

Michael, Piper Hans, ed. Cell culture technique in heart and vessel research. Berlin: Springer-Verlag, 1990.

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29

Merklinger, Sandra Lea. Progression and regression of pulmonary vascular disease related to smooth muscle cell apoptosis, S100A4/Mts1 and fibulin-5. 2005.

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30

Fleming, Ingrid, Brenda R. Kwak, and Merlijn J. Meens. The endothelial cell. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0006.

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The endothelium, a monolayer of cells that lines blood vessels, acts as a physical barrier between circulating blood and vascular smooth muscle cells. The purpose of this chapter is to provide a general overview on the structural heterogeneity of the endothelium. Moreover, the most important physiological functions of the vascular endothelium in blood vessels are discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and hypertension, are provided in other chapters of this book.
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31

Handa, Shivalika. Investigating smooth muscle cell marker gene expression in distinct regions of the mouse aorta during early atherosclerosis by microdissection and mRNA analysis. 2006.

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32

Muneer, Asif, and David Ralph. Priapism. Edited by David John Ralph. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0106.

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Priapism is rare and is a medical emergency. Ischaemic priapism is the commonest subtype with haematological abnormalities, psychotropic or recreational drug use and malignancy being the other common aetiologies. Emergency decompression of this compartment syndrome is required to preserve cavernosal smooth muscle function and this should ideally be performed as soon as possible. The degree of resultant erectile dysfunction is related to the duration of the priapism. Non-ischaemic priapism is an unregulated inflow of arterial blood, often as a result of perineal trauma and a lacerated cavernosal vessel. Selective arterial embolization should be performed and results are usually excellent. The final subtype is stuttering priapism, the cause of which is often unknown and a variety of methods will be discussed for its treatment.
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33

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.
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34

van Hinsbergh, Victor W. M. Physiology of blood vessels. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0002.

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This chapter covers two major fields of the blood circulation: ‘distribution’ and ‘exchange’. After a short survey of the types of vessels, which form the circulation system together with the heart, the chapter describes how hydrostatic pressure derived from the heartbeat and vascular resistance determine the volume of blood that is locally delivered per time unit. The vascular resistance depends on the length of the vessel, blood viscosity, and, in particular, on the diameter of the vessel, as formulated in the Poiseuille-Hagen equation. Blood flow can be determined in vivo by different imaging modalities. A summary is provided of how smooth muscle cell contraction is regulated at the cellular level, and how neuronal, humoral, and paracrine factors affect smooth muscle contraction and thereby blood pressure and blood volume distribution among tissues. Subsequently the exchange of solutes and macromolecules over the capillary endothelium and the contribution of its surface layer, the glycocalyx, are discussed. After a description of the Starling equation for capillary exchange, new insights are summarized(in the so-called glycocalyx cleft model) that led to a new view on exchange along the capillary and on the contribution of oncotic pressure. Finally mechanisms are indicated in brief that play a role in keeping the blood volume constant, as a constant volume is a prerequisite for adequate functioning of the circulatory system.
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35

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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36

Badimon, Lina, and Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Abstract:
Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.
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37

Whitworth, Caroline, and Stewart Fleming. Malignant hypertension. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0216.

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Malignant hypertension (MH) is recognized clinically by elevated blood pressure together with retinal haemorrhages or exudates with or without papilloedema (grades III or IV hypertensive retinopathy); and may constitute a hypertensive emergency or crisis when complicated by evidence of end-organ damage including microangiopathic haemolysis, encephalopathy, left ventricular failure, and renal failure. Though reversible, it remains a significant cause of end-stage renal failure, and of cardiovascular and cerebrovascular morbidity and mortality in developing countries.MH can complicate pre-existing hypertension arising from diverse aetiologies, but most commonly develops from essential hypertension. The absolute level of blood pressure appears not to be critical to the development of MH, but the rate of rise of blood pressure may well be relevant in the pathogenesis. The pathogenesis of this transformation remains unclear.The pathological hallmark of MH is the presence of fibrinoid necrosis (medial vascular smooth muscle cell necrosis and fibrin deposition within the intima) involving the resistance arterioles in many organs. Fibrinoid necrosis is not specific to MH and this appearance is seen in other conditions causing a thrombotic microangiopathy such as haemolytic uraemic syndrome, scleroderma renal crisis, antiphospholipid syndrome, and acute vascular rejection post transplant. MH can both cause a thrombotic microangiopathy (TMA) but can also complicate underlying conditions associated with TMA.The pathophysiological factors that interact to generate and sustain this condition remain poorly understood. Risk factors include Afro-Caribbean race, smoking history, younger age of onset of hypertension, previous pregnancy, and untreated hypertension associated with non-compliance or cessation of antihypertensive therapy.Evidence from clinical studies and animal models point to a central role for the intrarenal renin–angiotensin system (RAS) in MH; there is good evidence for renal vasoconstriction and activation of the renal paracrine RAS potentiating MH once established; however, there may also be a role in the predisposition of MH suggested by presence of increased risk conferred by an ACE gene polymorphism in humans and polymorphisms for both ACE and AT1 receptor in an animal model of spontaneous MH. Other vasoactive mediators such as the endothelin and the inflammatory response may be important contributing to and increasing endothelial damage. There have been no randomized controlled trials to define the best treatment approach, but progressive lowering of pressures over days is considered safest unless made more urgent by critical clinical state. It seems logical to introduce ACE inhibition cautiously and early, but in view of the risk of rapid pressure lowering some recommend delay.
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