**11. Integral atherogenesis**

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 atherosclerosis by increasing smooth muscle cell susceptibility to insulin-like growth fac‐ tor-1 mitogenic effects [6].

In such manner, distributional effects integrate as quantitative formulations of an atheroscler‐ otic plaque that re-characterizes dimensions of phenotype switching and formulates roles for transforming cell types. Various nuclear receptors contribute to macrophage cholesterol me‐

Attributes of Hypoxic Preconditioning Determine the Complicating Atherogenesis of Plaques

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

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Incremental involvement of the intima corresponds to a progression that spatially conforms to effects of a disturbed blood flow that interacts with the endothelium. Dysfunctionality of endothelial cells arises within contexts of such interface phenomena in the realization of the quantitative attributes of increasing hypoxic injury and as dictated by the an accumulation

Developmental parallels of involvement permit the destruction of the vascular intima that however promotes dimensions of aggregation of monocytes and the transformation to foam cells. In such manner, parameters of increasing involvement of the intima with atrophy of the tunica media progressively increases the abnormal flow of blood and promotes distur‐ bed reactivity of endothelial cells. It is such cyclical disturbance that increases also the sus‐

A conceptual realization of developmental events is suggestive of a series of parallel path‐ ways that coincidentally progress as overlapping systems of attempted reconstitution of pathways of possible recovery in the face of incremental destruction of the vascular wall. Monocyte recruitment into the vessel wall is a rate-limiting step in atherogenesis with a crit‐

In such events promotional permissiveness would prove a determining series of further pro‐ gression that calls into operative persistence the effects of hypoxia and of disturbed blood

Extension, both laterally and also deeply into the vascular wall, requires the activation of response elements such as the shear stress response element that augments the distribution‐ al disturbance of interaction of tonicity of the vascular wall with disturbed dynamics of

This phenomenon appears to augment further susceptibility to pro-inflammatory reactivity in the wake of an enlarging plaque that increasingly constitutes the phenotypic switching of such cell types as smooth muscle cells. Also, remodelling of the intima is both accumulative

Substantial reconstitution of the vessel wall, hence, is attempted in the form of replacement dynamics in the vascular wall in a manner that attempts the normalization, to some extent,

of proteoglycans and also modulatory in adapting to new blood flow dynamics.

ceptibility to progressive accumulation of lipoprotein within the vascular wall.

tabolism, which in turn keeps the arteries in a chronically inflamed state [26].

**13. Endothelial dysfunction**

of oxidized lipoprotein core.

**14. Permissiveness**

blood flow.

ical role played by reactive oxygen species [35].

flow that primarily target the endothelial cell bed.

The foam cells within the plaque are an expression of integrative participation within such schemes of complicating plaque formation as realized by such phenomena as lipid core accumulation, chemotaxis, paracrine secretion of growth factors and cytokines and the expres‐ sive effects of oxidized lipoproteins in particular. The distributional nature of disturbed blood flow is significant in the role of selective participation of injury to the overlying endothelial cells that become permeable to the inflow of lipoproteins within the vascular wall. Low density lipoproteins play a major role in initiating progressive atherosclerosis whereas high density lipoproteins suppress inflammation and thrombosis [1].

Hence, an overall series of dimensional agonists conform to and further establish the emer‐ gence of hypoxic influence in the quantitative formulation of the individual atherosclerotic plaque within a highly permissive micro-environment of vascular wall pathology. The sig‐ nificance of multi-component participation is symptomatic of the essential activation of en‐ dothelial cells that are at the interface with disturbed blood flow. Also, the accelerated or aggressive forms of atherogenesis seen in many forms of dyslipoproteinemias illustrate such phenomenon within parametric contexts of endothelial cell dysfunction.
