**8. Tunica intima**

The multi-component history of injury would account for a concordance influence in deter‐ mining the realization of initiating injury to the endothelium and to the distributional contri‐ butions for further different forms of injury to other components of the vascular wall.

Parameters of progression are differential contributors to the essential nature of atherogene‐ sis that is both dysfunctional and activating to such cell components as the endothelium. Es‐ trogens have potent antioxidant activity and reverse endoplasmic reticulum stress in endothelial cells [14]. The proximity of the tunica intima to both overlying endothelium and to tunica media promotes the interactivity of smooth muscle cells within paracrine and auto‐ crine systems of determining pathobiology. The significance attributed to such pathways as deposition of proteoglycan matrix within the intima proves a heterogeneity of involvement as significant characterization of multiple forms of progression of the individual atheroscler‐ otic plaque. In such manner, distributional dynamics within foci of involvement by athero‐ sclerosis allow for the emergence of parameters of progression that identifiably further promote permissive conditions of a quantitative nature in accumulation and chemotaxis of monocytes in particular.

ed with overlapping risk factors [8]. The overall dimensions of plaque evolution are hence highly complex, and such complexity is largely attributable to participants from the overly‐

Attributes of Hypoxic Preconditioning Determine the Complicating Atherogenesis of Plaques

http://dx.doi.org/10.5772/51127

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In spite of such considerations an essential role for hypoxia specifically affects the endotheli‐

The neovascularization at the base of the complicated atherosclerotic plaque may be an ex‐ pression of such overall effects of hypoxia that transforms accumulative phenomena of athe‐

The pro-inflammatory nature of plaques appears also expressive parameter of such hypoxia as a result of a neovascularity that further emerges as an over-riding phenomenon of per‐ missiveness in atherogenesis. In this regard Nuclear Factor-kappaB plays an orchestrating role in formulating multiple heterogeneous elements in evolutionary permissiveness. As HIV infected patients age, atherosclerosis has become an increasing cause of morbidity and

The directional promotion in development of the unstable plaque is therefore an expression of transformational dynamics that promotes the rupture of the overlying fibrous cap and the extrusion of the lipid core. The biophysics of such fibrous cap appears instrumental particu‐

The interplay of genetic factors with micro-environmental agonists is particularly significant

Such phenomenal increments play contributing roles of the overlying blood flow in redis‐ tributing lipoproteins and cholesterol within the vascular wall. The dimensions of the lipid core are themselves determining agonists in plaque rupture, and a high content of such lipid

Redistribution of attributes within the individual atherosclerotic plaque appears a promo‐ tional feature as pro-inflammatory effects and as plaque neovasculature. The hypoxic envi‐ ronment would account for permissive emergence of multi-component parameters that coordinate the characterization of the final complicated atherosclerotic plaque within di‐

The complicated atherosclerotic plaque as integral atherogenesis is an overall principal par‐ ticipation in the progression of a lesion that is both pro-inflammatory and enlarging. Ad‐ vanced glycation end-products are implicated in the pathogenesis of diabetes-associated

larly in the disruption of the junctional elements with the adjacent vascular wall.

in terms of the dynamics of lipid accumulation within the plaque [16].

core to over 40% of the overall plaque is significant in this regard.

mensions of accumulation of lipid and transformation to plaque rupture.

ing luminally disturbed blood flow.

**10. Neovascularization**

**11. Integral atherogenesis**

um and other components of the vascular wall.

rogenesis as complicated plaques that rupture into the lumen.

mortality, initiating immune and inflammatory responses [23].
