By Sarah Jane George, Jason Johnson
Protecting the main devastating ailment within the Western international, this guide and prepared reference presents a accomplished account of the various phases and elements within the improvement of the atherosclerotic plaque. every one bankruptcy is written via specialists within the box and highlights the function of particular mediators of atherosclerotic plaque improvement, in addition to power healing pursuits. a large number of this up to date info is conveyed when it comes to tables and schematic figures, in a without difficulty understandable demeanour. a must have for grasp and PhD scholars, researchers, MDs and academics in vascular biology and cardiology, in addition to for lecturers and scientists within the pharmaceutical undefined.
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Extra info for Atherosclerosis: Molecular and Cellular Mechanisms
Et al. (1992) A deﬁnition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the committee on vascular lesions of the council on arteriosclerosis, American Heart Association. Arterioscler. , 12 (1), 120–134. , et al. (1995) A deﬁnition of advanced types of atherosclerotic lesions and a histological classiﬁcation of atherosclerosis: a report from the committee on vascular lesions of the council on arteriosclerosis, American Heart Association. Arterioscler. Thromb.
CXCL9 and CXCL10 were induced locally and systemically in response to wire injury, resulting in enhanced recruitment of CXCR3+ cells, activation of mTORC1, generation of reactive oxygen species and induction of apoptosis. Furthermore, blockade of CXCR3 signaling led to a signiﬁcant reduction in intimal hyperplasia, suggesting a novel link between T cell stimulation and intimal SMC proliferation. A very recent report has documented an increase in blood pressure in CXCR3 knockout mice . The mechanism whereby deﬁciency of a single chemokine receptor causes hypertension remains to be determined, but this paper reminds us that chemokines and their receptors have many functions beside recruitment of inﬂammatory cells into atherosclerotic lesions.
Monocytes and macrophages display a high level of heterogeneity to allow them to specialize in particular functions. Many macrophage phenotypes have been identiﬁed and at least two of these (M1 and M2) have been shown to be present in atherosclerotic plaques. The phenotype expressed by a macrophage depends on the chemical signals used to induce macrophage differentiation. Th1 cytokines, such as IFN-γ, IL-1β and lipopolysaccharide, induce a “classical” activation proﬁle called M1. On the other hand, Th2 cytokines, such as IL-4 and IL-13, induce an “alternative” activation program called M2.