Guanghong Jia1,2, Annayya R Aroor3,4, Luis A Martinez-Lemus4,5,6, James R Sowers7,8,9,10. 1. Diabetes and Cardiovascular Research Center, University of Missouri School of Medicine, D109 Diabetes Center HSC, One Hospital Drive, Columbia, MO, 65212, USA. jiag@health.missouri.edu. 2. Research Service, Truman Memorial Veterans Hospital, Columbia, MO, 65201, USA. jiag@health.missouri.edu. 3. Diabetes and Cardiovascular Research Center, University of Missouri School of Medicine, D109 Diabetes Center HSC, One Hospital Drive, Columbia, MO, 65212, USA. 4. Research Service, Truman Memorial Veterans Hospital, Columbia, MO, 65201, USA. 5. Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, 65211, USA. 6. Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO, 65212, USA. 7. Diabetes and Cardiovascular Research Center, University of Missouri School of Medicine, D109 Diabetes Center HSC, One Hospital Drive, Columbia, MO, 65212, USA. sowersj@health.missouri.edu. 8. Research Service, Truman Memorial Veterans Hospital, Columbia, MO, 65201, USA. sowersj@health.missouri.edu. 9. Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, 65211, USA. sowersj@health.missouri.edu. 10. Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, MO, 65212, USA. sowersj@health.missouri.edu.
Abstract
PURPOSE OF REVIEW: Increased arterial stiffness, an abnormal structural and functional change in the vascular wall, is a precursor for hypertension, coronary heart disease, stroke, and associated cardiovascular disease (CVD). The aim of this paper is to review the etiology of arterial stiffening and potential therapeutic approaches to modulate arterial fibrosis and stiffness. RECENT FINDINGS: The Framingham Heart Study demonstrated that arterial stiffness is an independent predictor of CVD and related morbidity and mortality. Dysfunction of endothelial cells, vascular smooth muscle cells, extracellular matrix, and other functional elements of the vessel wall contribute to underlying pathophysiology of increased arterial stiffness. An activated renin-angiotensin-aldosterone system, oxidative stress, abnormal peri-vascular adipose tissue, inflammation, and increased sympathetic nervous system activity are associated with the development and progression of arterial fibrosis, stiffening, and associated CVD. In this review, we will discuss the structural and function changes and mechanisms of the vessel wall in arterial stiffness and provide potential therapeutic strategies.
PURPOSE OF REVIEW: Increased arterial stiffness, an abnormal structural and functional change in the vascular wall, is a precursor for hypertension, coronary heart disease, stroke, and associated cardiovascular disease (CVD). The aim of this paper is to review the etiology of arterial stiffening and potential therapeutic approaches to modulate arterial fibrosis and stiffness. RECENT FINDINGS: The Framingham Heart Study demonstrated that arterial stiffness is an independent predictor of CVD and related morbidity and mortality. Dysfunction of endothelial cells, vascular smooth muscle cells, extracellular matrix, and other functional elements of the vessel wall contribute to underlying pathophysiology of increased arterial stiffness. An activated renin-angiotensin-aldosterone system, oxidative stress, abnormal peri-vascular adipose tissue, inflammation, and increased sympathetic nervous system activity are associated with the development and progression of arterial fibrosis, stiffening, and associated CVD. In this review, we will discuss the structural and function changes and mechanisms of the vessel wall in arterial stiffness and provide potential therapeutic strategies.
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