Titlebook: Mechanisms of Vascular Defects in Diabetes Mellitus; C.C. Kartha,Surya Ramachandran,Radhakrishna M. Pil Book 2017 Springer International P

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Anita Mahadevan,Shankar S. Krishna M.D., F.A.M.S., F.N.A.Sc.

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The Global Burden of Diabetes and Its Vascular Complicationsin low and middle-income nations that have rapidly improved their economy and adopted a ‘westernized’ life style. The worldwide explosion of diabetes also increases the propensity for developing both micro and macro vascular complications and this result in a huge burden due to mobility and mortalit

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Vascular Remodeling in Diabetes Mellitusultiple pathways resulting in profound changes in the structure and function of all layers of the arterial wall. Vascular remodeling causes endothelial dysfunction, increased extracellular matrix formation, vascular smooth muscle cell proliferation and vascular calcification. This results in reduced

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Pathogenesis of the Plaque Vulnerability in Diabetes Mellitus. Atherosclerosis and acute coronary syndrome are more common in diabetes mellitus. Hyperglycemia and hypercholesterolemia in diabetes predispose the arteries to plaque development. Smoking, hypertension, male sex, and family history or genetic susceptibility are other predisposing factors for plaqu

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Endothelial Dysfunction in Diabetesc patients. The initiating cause of these diseases is endothelial dysfunction, due to presence of multiple risk factors such as, insulin resistance, dyslipidemia, inflammation and hyperglycemia. This chapter summarizes our current understanding of molecular mechanisms that contribute to endothelial

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Smooth Muscle Cells in Diabetes Mellitusdisease whereas the macrovascular disease is significantly associated with the mortality in the diabetic patients. The macrovascular disease, also known as diabetes-accelerated atherosclerosis is promoted by the interplay of multiple factors. These biochemical and molecular parameters predominantly

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Monocyte Factors in Pathogenesis of Vascular Lesions in Diabetes blood. The resulting recruitment of monocytes, their differentiation into a pro-inflammatory phenotype and formation of foam cells in the sub endothelial space are the hallmark of early atherogenesis. This process is orchestrated by a range of cytokines, chemokines and chemoattractants, which influ