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Books on the topic 'Atherosclerosis – Pathogenesis'

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Published: 4 June 2021
Last updated: 20 February 2023

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1

Haverich, Axel, and Erin Colleen Boyle. Atherosclerosis Pathogenesis and Microvascular Dysfunction. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-20245-3.

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2

Modified lipoproteins in the pathogenesis of atherosclerosis. Austin: R.G. Landes Co., 1994.

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3

Subbiah, M. T. R., 1942-, ed. Atherosclerosis: A pediatric perspective. Boca Raton, Fla: CRC Press, 1989.

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4

N, Diana John, ed. Tobacco smoking and atherosclerosis: Pathogenesis and cellular mechanisms. New York: Plenum Press, 1990.

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5

L, Malmendier Claude, and Alaupovic P, eds. Eicosanoids, apolipoproteins, lipoprotein particles, and atherosclerosis. New York: Plenum, 1988.

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6

1944-, Shepherd J., Packard Christopher J, and Brownlie Sheena M, eds. Lipoproteins and the pathogenesis of atherosclerosis: Proceedings of the International Symposium on Lipoproteins and the Pathogenesis of Atherosclerosis, Gleneagles, Perthshire, 24-27 February 1991. Amsterdam: Excerpta Medica, 1991.

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7

Workshop on Carotid Artery Plaques (1987 Gutersloh, Germany). Carotid artery plaques: Pathogenesis, development, evaluation, treatment. Edited by Hennerici M, Sitzer G, Weger Hans-Dieter, Bertelsmann Stiftung (Gütersloh Germany), and Universität Düsseldorf. Dept. of Neurology. Basel: Karger, 1988.

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8

P, Gallos Alice, and Jones Margaret L, eds. Angina pectoris: Etiology, pathogenesis, and treatment. New York: Nova Science Publishers, 2008.

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9

Boris, Draznin, and Eckel Robert H, eds. Diabetes and atherosclerosis: Molecular basis and clinical aspects. New York: Elsevier, 1993.

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10

International Dresden Lipid Symposium (9th 1997 Dresden, Germany). Advances in lipoprotein and atherosclerosis researh, diagnostic and treatment: Proceedings of the 9th International Dresden Lipid Symposium, held at Dresden, June 27-29, 1997. Edited by Hanefeld Markolf. Jena: G. Fischer, 1998.

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11

International Dresden Lipid Symposium (7th 1991 Dresden, Germany). Advances in lipoprotein and atherosclerosis research, diagnostics and treatment: Proceedings of the 7th International Dresden Lipid Symposium 1991 Held at Dresden, June 9-11, 1991. Edited by Dude H, Hanefeld Markolf, and Jaross W. Stuttgart: Gustav Fischer Verlag Jena, 1991.

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12

Altschul Symposium (1st 1990 Saskatoon, Sask.). Atherosclerosis: Cellular and molecular interactions in the artery wall. New York: Plenum Press, 1991.

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13

The lipid hypothesis of atherogenesis. Austin: R.G. Landes, 1993.

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14

Orr, A. Wayne, Brijesh M. Patel, and Arif Yurdagul Jr. Pathogenesis of Atherosclerosis. Morgan & Claypool Publishers, 2014.

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15

Hypercholesterolemia & Atherosclerosis: Pathogenesis & Prevention. Books on Demand, 1987.

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16

Haverich, Axel, and Erin Colleen Boyle. Atherosclerosis Pathogenesis and Microvascular Dysfunction. Springer International Publishing AG, 2020.

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17

Haverich, Axel, and Erin Colleen Boyle. Atherosclerosis Pathogenesis and Microvascular Dysfunction. Springer International Publishing AG, 2019.

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18

Wiklund, Olov, and Jan Borén. Pathogenesis of atherosclerosis: lipid metabolism. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0011.

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Lipids are carried in plasma as microparticles, lipoproteins, composed of a core of hydrophobic lipids and a surface of amphipathic lipids. In addition, the particles carry proteins (i.e. apolipoproteins). The proteins have key functions in the metabolism as receptor ligands, enzymes or activators. Lipoproteins are classified based on density into: chylomicrons, VLDL, IDL, LDL, and HDL. Retention of apoB-containing lipoproteins (LDL, IDL, and VLDL) in the arterial intima is the initiating event in the development of atherosclerosis. Retention is mediated by binding of apoB to structural proteoglycans in the intima. Increased plasma concentration of apoB-containing lipoproteins is the main risk factor for atherosclerotic cardiovascular disease (CVD) and the causative role of LDL has been demonstrated in several studies. Lp(a) is a subclass of LDL and elevated Lp(a) is an independent risk-factor, primarily genetically mediated. Genetic data support that high Lp(a) causes atherosclerosis. Elevated triglycerides in plasma are associated with increased risk for CVD. Whether triglycerides directly induce atherogenesis is still unclear, but current data strongly support that remnant particles from triglyceride-rich lipoproteins are causal. HDL are lipoproteins that have been considered to be important for reversed cholesterol transport. Low HDL is a strong risk-factor for CVD. However, the causative role of HDL is debated and intervention studies to raise HDL have not been successful. Reduction of LDL is the main target for prevention and treatment, using drugs that inhibit the enzyme HMG-CoA reductase, i.e. statins. Other drugs for LDL reduction and to modify other lipoproteins may further reduce risk, and new therapeutic targets are explored.
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19

Harats, D. Atherosclerosis and Autoimmunity. Elsevier Science Pub Co, 2001.

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20

Harats, D., G. Wick, and Y. Shoenfeld. Atherosclerosis and Autoimmunity. Elsevier Science & Technology Books, 2001.

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21

1922-, Steinberg Daniel, and Olefsky Jerrold M, eds. Hypercholesterolemia and atherosclerosis: Pathogenesis and prevention. New York: Churchill Livingstone, 1987.

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22

Weber, Peter C. Atherosclerosis: Its Pathogenesis and the Role of Cholesterol (Atherosclerosis Reviews). Raven Pr, 1991.

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23

Mitrovska, Slavica, Silvana Jovanova, Inge Matthiesen, and Christian Libermans. Atherosclerosis: Understanding Pathogenesis and Challenge for Treatment. Nova Science Publishers, Incorporated, 2009.

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24

Yehuda, Shoenfeld, Harats Dror, and Wick G, eds. Atherosclerosis and autoimmunity. Amsterdam: Elsevier, 2001.

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25

C, Weber Peter, Leaf Alexander 1920-, and Bayer AG "International Workshop on Atherosclerosis" (2nd : 1990 : Faro, Portugal), eds. Atherosclerosis: Its pathogenesis and the role of cholesterol. New York: Raven Press, 1991.

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26

Diana, John N. Tobacco Smoking and Atherosclerosis: Pathogenesis And Cellular Mechanisms. Springer, 2012.

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27

Orr, A. Wayne, Arif Yurdagul Jr, and Brijesh M. Patel. Pathogenesis of Atherosclerosis: From Cell Biology to Therapeutics. Morgan & Claypool Life Science Publishers, 2014.

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28

Diana, John N. Tobacco Smoking and Atherosclerosis: Pathogenesis and Cellular Mechanisms. Springer London, Limited, 2013.

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29

Monaco, Claudia, and Esther Lutgens. Atherosclerosis—a short history. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0010.

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The pathogenesis of human atherosclerotic lesions has long been debated and is still evolving nowadays. First conceptualized as chronically evolving degenerative disease initiating in the mother’s womb, then increasingly accepted as a dynamic process causing severe acute complications that jeopardize the blood flow to the heart. Evolution of the hypothesis mirrored the progress of cellular and molecular biology, leading to progressive broadening of the understanding of cell types and molecules involved in atherogenesis. This chapter describes the current histopathological view on the pathogenesis of atherosclerosis, and touches on a historical perspective weaving in the fundamental discoveries that still influence the perception of this disease in humans.
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30

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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31

Cholesterol transport systems and their relation to atherosclerosis. Berlin: Springer-Verlag, 1989.

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32

1933-, Meyer Philippe, Marche Pierre, Fondation Princesse Liliane. International Scientific Council., and Argenteuil Symposium (12th : 1987 : Brussels, Belgium), eds. Blood cells and arteries in hypertension and atherosclerosis. New York: Raven Press, 1989.

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33

Sitzer, G., and M. Hennerici. Carotid Artery Plaques: Pathogenesis, Development, Evaluation, and Treatment. S Karger Pub, 1988.

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34

Titov. Phylogenetic theory of the general pathology. Pathogenesis of a civilization diseases. Atherosclerosis. Infra-M Academic Publishing House, 2013. http://dx.doi.org/10.12737/858.

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35

(Editor), Claude L. Malmendier, and Petar Alaupovic (Editor), eds. Eicosanoids, Apolipoproteins, Lipoprotein Particles, and Atherosclerosis (Advances in Experimental Medicine and Biology). Springer, 1989.

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36

Steinberg, Daniel. Hypercholesterolemia and Atherosclerosis: Pathogenesis and Prevention (Contemporary Issues in Endocrinology and Metabolism, Vol 3). Churchill Livingstone, 1987.

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37

(Editor), Sergey Fedoroff, Gary D. Burkholder (Editor), Avrum I. Gotlieb (Editor), and B. Lowell Langille (Editor), eds. Atherosclerosis: Cellular and Molecular Interactions in the Artery Wall (Altschul Symposia Series). Springer, 1991.

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38

Klingenberg, Roland, and Ulf Müller-Ladner. Mechanisms of inflammation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0270.

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This chapter provides a brief summary of the immune pathogenesis of atherosclerosis, highlighting shared features with inflammatory pathways in rheumatoid arthritis (RA) described in detail in Chapter 25.4. RA constitutes a prototype autoimmune disease primarily affecting the joints but also the heart and vessels associated with increased cardiovascular mortality. Recent years have produced a wealth of novel insights into the diversity of immune cell types which either propagate or dampen inflammation in atherogenesis. Expansion of this inherent anti-inflammatory component carried by regulatory T cells may constitute a new therapeutic target to harness the progression of atherosclerotic cardiovascular disease. Among the various inflammatory mediators involved in RA pathology, cytokines (tumour necrosis factor-α‎ and interleukin-6) have gained major interest as therapeutic targets with approved therapies available. In light of the many common features in the pathogenesis of RA and atherosclerosis, these biologics are currently being evaluated in cardiovascular patients. The recently published CANTOS trial showed that IL-1 inhibition reduced adverse cardiovascular events in patients with coronary artery disease demonstrating that inflammation is a genuine therapeutic target. The near future will provide more information whether inflammation is a bona fide cardiovascular risk factor based on completion of several clinical trials using anti-inflammatory approaches in patients with both cardiovascular disease and rheumatoid arthritis.
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39

1932-, Yoshida Yōji, Nihon Dōmyaku Kōka Gakkai, and International Symposium on the Role of Blood Flow in Atherogenesis (1987 : Hyōgo-ken, Japan), eds. Role of blood flow in atherogenesis: Proceedings of the international symposium, Hyogo, October 1987. Tokyo: Springer-Verlag, 1988.

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40

Stehbens, William E. Lipid Hypothesis Of Atherogenesis. Eurekah.Com Inc, 2004.

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41

van Thiel, Bibi S., I. van der Pluijm, Roland Kanaar, A. H. Jan Danser, and Jeroen Essers. Structure and cell biology of the vessel wall. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0001.

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The purpose of this chapter is to provide a general overview on the structure and composition of blood vessels. Moreover, the cellular constituents of the vessel wall, as well as the different types of blood vessels, are discussed. In addition the effect of ageing on the vascular wall and its role in the pathogenesis of vascular disease is discussed. More detailed insights into the pathogenesis of specific diseases, including atherosclerosis and aneurysms, are provided in other chapters of this book.
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42

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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43

Gu, Wenduo, Yao Xie, and Qingbo Xu. Animal models to study pathophysiology of the vasculature. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0005.

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Animal models are designed to be preliminary tools for a better understanding of the pathogenesis, improvement in diagnosis, prevention, and therapy of vascular diseases in humans. Animal models are easily manageable, as compounding effects of dietary and environmental factors can be controlled experimentally. Blood vessel samples can be taken for detailed experimental and biomolecular examination. A thorough understanding of the animal models used is necessary and complete analysis must be validated so that the data can be extrapolated to humans. There are several species that are used for studying vascular pathophysiology, including mice, rats, rabbits, and pigs. Attracted by the well-defined genetic systems, a number of investigators have begun to use the mouse as an experimental system for arteriosclerosis research. Because vascular disorder is a complicated disease, which includes spontaneous (native) atherosclerosis, transplant arteriosclerosis, vein graft atherosclerosis, and angioplasty-induced restenosis, several models for studying all types of vascular disease have recently been established. Using these animal models, much knowledge concerning the pathogenesis of the disease and therapeutic intervention has been gained. This chapter will not attempt to cover all aspects of animal models, but will rather focus on the major progress in understanding the pathophysiology of the vasculature, the (dis)advantages of a variety of models, and how specific models can be appropriately chosen for different purposes of study.
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44

Guzik, Tomasz J., and Rhian M. Touyz. Vascular pathophysiology of hypertension. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0019.

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Hypertension is a multifactorial disease, in which vascular dysfunction plays a prominent role. It occurs in over 30% of adults worldwide and an additional 30% are at high risk of developing the disease. Vascular pathology is both a cause of the disease and a key manifestation of hypertension-associated target-organ damage. It leads to clinical symptoms and is a key risk factor for cardiovascular disease. All layers of the vascular wall and the endothelium are involved in the pathogenesis of hypertension. Pathogenetic mechanisms, whereby vascular damage contributes to hypertension, are linked to increased peripheral vascular resistance. At the vascular level, processes leading to change sin peripheral resistance include hyper-contractility of vascular smooth muscle cells, endothelial dysfunction, and structural remodelling, due to aberrant vascular signalling, oxidative and inflammatory responses. Increased vascular stiffness due to vascular remodelling, adventitial fibrosis, and inflammation are key processes involved in sustained and established hypertension. These mechanisms are linked to vascular smooth muscle and fibroblast proliferation, migration, extracellular matrix remodelling, calcification, and inflammation. Apart from the key role in the pathogenesis of hypertension, hypertensive vasculopathy also predisposes to atherosclerosis, another risk factor for cardiovascular disease. This is linked to increased transmural pressure, blood flow, and shear stress alterations in hypertension, as well as endothelial dysfunction and vascular stiffness. Therefore, understanding the mechanisms and identifying potential novel treatments targeting hypertensive vasculopathy are of primary importance in vascular medicine.
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45

Speer, Thimoteus, and Danilo Fliser. Abnormal endothelial vasomotor and secretory function. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0113.

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The endothelium plays a crucial role in the maintenance of vascular integrity and function. Nitric oxide produced by endothelial cells is a key player, inducing relaxation of vascular smooth muscle cells, inhibition of vascular inflammation, and prevention of coagulatory activation. Chronic kidney disease (CKD) is characterized by deterioration of different protective endothelial properties, collectively described as endothelial dysfunction. Several factors such as methylarginines, modified lipoproteins, and other substances that accumulate may be involved in the pathogenesis of endothelial dysfunction of CKD. Endothelial dysfunction is suggested to be the first critical step in the initiation of atherosclerosis. Clinical assessment of endothelial function may become important in recognition of patients with increased cardiovascular risk. Beside several invasive and non-invasive methods to assess endothelial function in vivo, measurement of circulating (bio)markers may be useful for the evaluation of endothelial dysfunction.
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46

Dey, Ida Dzifa, and David Isenberg. Systemic lupus erythematosus—management. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0118.

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Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease with varied presentation and a disease course characterized by remission and flares. Over the last 50 years, the prognosis of SLE has improved considerably. The introductions of corticosteroids and later of cytotoxic drugs, dialysis, and renal transplantation were the major contributors to this improvement. Nevertheless, the treatment and general management of lupus continues to present a challenge. While lupus may, for some patients, represent a relatively mild set of problems, many others require large doses of immunosuppressive drugs, which carry long-term concerns about side effects. New immunotherapeutic drugs, with actions more closely targeted to the immune cells and molecules involved in the pathogenesis of SLE, are being introduced and the future looks promising. The role of early atherosclerosis and cardiovascular disease as a cause of death in patients with SLE is increasingly recognized and will present further challenges in the future.
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47

Dey, Ida Dzifa, and David Isenberg. Systemic lupus erythematosus—management. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0118_update_003.

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Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease with varied presentation and a disease course characterized by remission and flares. Over the last 50 years the prognosis of SLE has improved considerably. The introductions of corticosteroids and later of cytotoxic drugs, dialysis, and renal transplantation were the major contributors to this improvement. Nevertheless, the treatment and general management of lupus continues to present a challenge. While lupus may, for some patients, represent a relatively mild set of problems, many others require large doses of immunosuppressive drugs, which carry long-term concerns about side effects. New immunotherapeutic drugs, with actions more closely targeted to the immune cells and molecules involved in the pathogenesis of SLE, are being introduced and the future looks promising. The role of early atherosclerosis and cardiovascular disease as a cause of death in patients with SLE is increasingly recognized and will present further challenges in the future.
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48

Dhaun, Neeraj, and David J. Webb. Endothelins and their antagonists in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0114_update_001.

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The endothelins (ETs) are a family of related peptides of which ET-1 is the most powerful endogenous vasoconstrictor and the predominant isoform in the cardiovascular and renal systems. The ET system has been widely implicated in both cardiovascular disease and chronic kidney disease (CKD). ET-1 contributes to the pathogenesis and maintenance of hypertension and arterial stiffness, as well endothelial dysfunction and atherosclerosis. By reversal of these effects, ET antagonists, particularly those that block ETA receptors, may reduce cardiovascular risk. In CKD patients, antagonism of the ET system may be of benefit in improving renal haemodynamics and reducing proteinuria, effects seen both in animal models and in some human studies. Data suggest a synergistic role for ET receptor antagonists with angiotensin-converting enzyme inhibitors in lowering blood pressure, reducing proteinuria, and in animal models in slowing CKD progression. However, in clinical trials, fluid retention or cardiac failure has caused concern and these agents are not yet ready for general use for risk reduction in CKD.
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