By Hong Wang, Cam Patterson
Comprehensive and in-depth in its coverage, Atherosclerosis: mobile, Molecular & Biochemical Mechanism and Novel Therapy reports the new growth in atherosclerosis study and gives innovative views from specialists within the box. Written through a world group of authors together with best physician-scientists, study specialists and physicians, chapters are divided into 4 significant sections, protecting hazard elements, mobile and molecular mechanisms, biochemical mechanisms and novel and destiny therapeutics.
Atherosclerosis: mobile, Molecular & Biochemical Mechanism and Novel Therapy analyses fresh development from either conceptual and technological views, suggesting new instructions for atherosclerosis examine and therapy for a turning out to be inhabitants of researchers and clinicians in cardiovascular and comparable fields.
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Additional resources for Atherosclerosis: Risks, Mechanisms, and Therapies
51. , et al. (2011) Functional and pathological roles of the 12-and 15-lipoxygenases. Prog Lipid Res 50(1): 115–131. 52. , et al. (2006) Enhanced proatherogenic responses in macro phages and vascular smooth muscle cells derived from diabetic db/db mice. Diabetes 55:2611–2619. 53. , et al. (2011) Diabetes adversely affects macrophages during atherosclerotic plaque regression in mice. Diabetes 60:1759–1769. 3 Glycation, Inflammation and RAGE: Mechanisms Contributing to the Accelerated Atherosclerosis of Diabetes Ravichandran Ramasamy, Shi Fang Yan, and Ann Marie Schmidt Diabetes Research Program, Division of Endocrinology, Department of Medicine, New York University Langone Medical Center, New York, NY, USA Introduction In both type 1 and type 2 diabetes, a major cause of morbidity and mortality is accelerated cardiovascular disease, manifested as increased incidence and severity of heart attacks and strokes .
Angiotensin II exposure results in oxidation of Src kinase through a Nox4-dependent activity —an effect that increases Src enzymatic activity and VSMC proliferation and migration. Other studies that are relevant to diabetes have shown that hyperglycemia enhances insulin-like growth factor I (IGF-1)-stimulated Src activation by increasing Nox4 expression . Under these conditions, IGF-1 stimulation leads to the recruitment of the p22 phox subunit to NOX4, resulting in enhanced Src oxidation and IGF-1stimulated VSMC migration and proliferation.
Young SG. (1993) Familial hypobetalipoproteinemia. Journal of Lipid Research 34, 521–541. 27. Cohen J, Pertsemlidis A, Kotowski IK, Graham R, Garcia CK, Hobbs HH. (2005) Low LDL cholesterol in individuals of African descent resulting from frequent nonsense mutations in pcsk9. Nature Genetics 37, 161–165. 28. Kotowski IK, Pertsemlidis A, Luke A, et al. (2006) A spectrum of pcsk9 alleles contributes to plasma levels of low-density lipoprotein cholesterol. American Journal of Human Genetics 78, 410–422.