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Cardiovascular disease (CVD) is currently the largest cause of death worldwide. World Health Organisation data [1] suggest that one-third, 17.1 million, of all deaths in 2004 were attributable to CVD. The majority of these relate to situations of coronary artery disease, stroke, hypertension and/or peripheral artery dis- ease. A feature common to each of these conditions is that alter- ation of vascular structure and/or function is a prominent contrib- utor to the CVD risk. It is timely, therefore, for this review series to bring together expert scientific and clinical expertise to assess the role of the vascular system in health and disease. As befits the remit of the Journal of Cellular and Molecular Medicine as a conduit for reporting translational medicine, the series will cover a research base from the scientific to the clinical, the in vitro to the in vivo. Of course, it would be impossible to sup- ply an exhaustive overview of all important research in this area without occupying several whole journal issues. Of necessity, there- fore, the review series will be focussed and the areas to be dis- cussed are three-fold. First, the molecular mechanisms that regulate the physiological constriction and dilation of arteries and arterioles are key components that are likely to be targeted either by the insult associated with CVD or by the intended therapeutic treatment for CVD. This will encompass consideration of the intracellular Ca 2 regulatory signalling pathways, the role of the endothelium, smooth muscle and extracellular matrix. Second, and analogously to the first point, alterations in arterial structure and function may predicate CVD onset or may be attractive pathways for beneficial intervention. The impact of alterations of cell growth, motility and altered pheno- type, and the correlation of disease risk with vessel wall mineraliza- tion, will be addressed. Third, a discussion of the benefits of various therapeutic strategies currently in clinical practice for treating CVD that target amelioration of altered vascular function and/or remodel- ling. Particular attention will be given to such strategies in the treat- ment of hypertensive and diabetic patients, whether central (large artery) or peripheral (small, resistance) arterial systems are most affected and the importance of organ-specific changes associated with CVD and particular treatment options [2–4]. WHO data also estimate that by 2030 there will have been a 27% increase in the numbers dying from CVD [1]. This may in large part be related to the forecasts of health and socioeconomic time bombs associated with rising rates of obesity and diabetes and, albeit somewhat counter-intuitive, a population of prolonged age [4–6]. Thus, in spite of the many advances in our understanding of vascular physiology and vasculopathology that the review series will high- light, it should also be apparent that there is a continued need to tailor, improve and invent new strategies for treating vascular dysfunction in CVD. As such, all the review authors will gaze in to their looking glasses and look forward to what they consider will be the key areas of advancement in their field for the next 5–10 years. In this regard it is of note that modelling the cost-effectiveness of large-scale interventions is becoming a prevalent consideration [7–8]. References 1. World Health Organisation http://www.who. int/mediacentre/factsheets/fs317/en/index. html 2. Agabiti-Rosei E, Heagerty AM, Rizzoni D. Effects of antihypertensive treatment on small artery remodelling. J Hypertens. 2009; 27: 1107–14. 3. Touyz RM, Schiffrin EL. Signal transduction mechanisms mediating the physiological and pathophysiological actions of angiotensin II in vascular smooth muscle cells. Pharmacol Rev. 2000; 52: 639–72. 4. Williams B, Lacy PS, Cruickshank JK, et al. Impact of statin therapy on central aortic pressures and hemodynamics: principal results of the Conduit Artery Function Evaluation-Lipid-Lowering Arm (CAFE-LLA) Study. Circulation. 2009; 119: 53–61. 5. Nemes A, Gavalier H, Csajbok E, et al. Obesity is associated with aortic enlargement and increased stiffness: an echocardiographic study. Int J Cardiovasc Imaging. 2008; 24: 165–71. 6. Heagerty AM, Mallion JM. (2009) Olmesartan medoxomil in elderly patients with essential or isolated systolic hyperten- sion: efficacy and safety data from clinical trials. Drugs Aging. 2009; 26: 61–76. 7. Mihaylova B, Briggs A, Armitage J, et al. Cost-effectiveness of simvastatin in people at different levels of vascular disease risk: eco- nomic analysis of a randomised trial in 20,536 individuals. Lancet. 2005; 365: 1779–85. 8. Heart Protection Study Collaborative Group. Statin cost-effectiveness in the United States for people at different vascular risk levels. Circ Cardiovasc Qual. Outcomes. 2009; 2: 65–72. Vascular function in health and disease Review Series Guest Editor Prof. Michael Taggart a, * a Institute of Cellular Medicine, Newcastle University, UK J. Cell. Mol. Med. Vol 14, No 5, 2010 pp. 1017 © 2010 The Author Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd doi: 10.1111/j.1582-4934.2010.01050.x Editorial Foreword *Correspondence to: Michael TAGGART, Institute of Cellular Medicine, 3 rd Floor Leech Building, Framlington Place, Newcastle University, Newcastle upon Tyne, UK NE2 4HH. Tel.: 44 (0) 191 222 6988 Fax: 44 (0) 191 222 5066 E-mail: [email protected]

Vascular function in health and disease Review Series

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Cardiovascular disease (CVD) is currently the largest cause ofdeath worldwide. World Health Organisation data [1] suggestthat one-third, 17.1 million, of all deaths in 2004 were attributableto CVD. The majority of these relate to situations of coronaryartery disease, stroke, hypertension and/or peripheral artery dis-ease. A feature common to each of these conditions is that alter-ation of vascular structure and/or function is a prominent contrib-utor to the CVD risk. It is timely, therefore, for this review series tobring together expert scientific and clinical expertise to assess therole of the vascular system in health and disease.

As befits the remit of the Journal of Cellular and MolecularMedicine as a conduit for reporting translational medicine, theseries will cover a research base from the scientific to the clinical,the in vitro to the in vivo. Of course, it would be impossible to sup-ply an exhaustive overview of all important research in this areawithout occupying several whole journal issues. Of necessity, there-fore, the review series will be focussed and the areas to be dis-cussed are three-fold. First, the molecular mechanisms that regulatethe physiological constriction and dilation of arteries and arteriolesare key components that are likely to be targeted either by the insultassociated with CVD or by the intended therapeutic treatment forCVD. This will encompass consideration of the intracellular Ca2�

regulatory signalling pathways, the role of the endothelium, smoothmuscle and extracellular matrix. Second, and analogously to the firstpoint, alterations in arterial structure and function may predicate

CVD onset or may be attractive pathways for beneficial intervention.The impact of alterations of cell growth, motility and altered pheno-type, and the correlation of disease risk with vessel wall mineraliza-tion, will be addressed. Third, a discussion of the benefits of varioustherapeutic strategies currently in clinical practice for treating CVDthat target amelioration of altered vascular function and/or remodel-ling. Particular attention will be given to such strategies in the treat-ment of hypertensive and diabetic patients, whether central (largeartery) or peripheral (small, resistance) arterial systems are mostaffected and the importance of organ-specific changes associatedwith CVD and particular treatment options [2–4].

WHO data also estimate that by 2030 there will have been a 27%increase in the numbers dying from CVD [1]. This may in large partbe related to the forecasts of health and socioeconomic time bombsassociated with rising rates of obesity and diabetes and, albeitsomewhat counter-intuitive, a population of prolonged age [4–6].Thus, in spite of the many advances in our understanding of vascularphysiology and vasculopathology that the review series will high-light, it should also be apparent that there is a continued need to tailor,improve and invent new strategies for treating vascular dysfunctionin CVD. As such, all the review authors will gaze in to their lookingglasses and look forward to what they consider will be the key areasof advancement in their field for the next 5–10 years. In this regardit is of note that modelling the cost-effectiveness of large-scaleinterventions is becoming a prevalent consideration [7–8].

References1. World Health Organisation http://www.who.

int/mediacentre/factsheets/fs317/en/index.html

2. Agabiti-Rosei E, Heagerty AM, Rizzoni D.Effects of antihypertensive treatment onsmall artery remodelling. J Hypertens. 2009;27: 1107–14.

3. Touyz RM, Schiffrin EL. Signal transduction mechanisms mediating thephysiological and pathophysiologicalactions of angiotensin II in vascular smoothmuscle cells. Pharmacol Rev. 2000; 52:639–72.

4. Williams B, Lacy PS, Cruickshank JK, et al.Impact of statin therapy on central aorticpressures and hemodynamics: principalresults of the Conduit Artery FunctionEvaluation-Lipid-Lowering Arm (CAFE-LLA)Study. Circulation. 2009; 119: 53–61.

5. Nemes A, Gavalier H, Csajbok E, et al. Obesity is associated with aorticenlargement and increased stiffness: anechocardiographic study. Int J CardiovascImaging. 2008; 24: 165–71.

6. Heagerty AM, Mallion JM. (2009)Olmesartan medoxomil in elderly patients

with essential or isolated systolic hyperten-sion: efficacy and safety data from clinicaltrials. Drugs Aging. 2009; 26: 61–76.

7. Mihaylova B, Briggs A, Armitage J, et al.Cost-effectiveness of simvastatin in people atdifferent levels of vascular disease risk: eco-nomic analysis of a randomised trial in 20,536individuals. Lancet. 2005; 365: 1779–85.

8. Heart Protection Study CollaborativeGroup. Statin cost-effectiveness in theUnited States for people at different vascularrisk levels. Circ Cardiovasc Qual. Outcomes.2009; 2: 65–72.

Vascular function in health and

disease Review Series

Guest Editor

Prof. Michael Taggart a, *

a Institute of Cellular Medicine, Newcastle University, UK

J. Cell. Mol. Med. Vol 14, No 5, 2010 pp. 1017

© 2010 The AuthorJournal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd

doi:10.1111/j.1582-4934.2010.01050.x

Editorial Foreword

*Correspondence to: Michael TAGGART,Institute of Cellular Medicine, 3rd Floor Leech Building, Framlington Place,Newcastle University, Newcastle upon Tyne, UK NE2 4HH.

Tel.: �44 (0) 191 222 6988Fax: �44 (0) 191 222 5066E-mail: [email protected]