**5. Progression**

In such manner, the promotional distributional significance of concurrent foci of injury is paramount parameter in inducing the characterization of lesions that essentially progress. Toll-like receptor signalling may link chronic inflammation with cardiovascular disease pro‐ gression and immune activation [31].

It is significant to view the parameters of quantitative nature in the development of individ‐ ual lesions that hemodynamically are closely related often to disturbed blood flow at vascu‐ lar branch points.

It is with referential background components of various identifiable elements of the vascular wall that atherogenesis proves an integrative phenomenon of progression in its own right. High density lipoprotein particle functionality is at least as important as HDL-C levels due to effects on inflammation, hemostasis and apoptosis [22].

The individual participating roles played by such processes as monocyte rolling and subse‐ quent firm adhesion to endothelial cells helps characterize specific attributes of the activated or dysfunctional endothelium. The decreased production of nitric oxide by dysfunctional endothelium is a prototype example of distributional nature in denoting a systemic partici‐ pation of further ongoing transformation in phenotype characterization of cellular compo‐ nents of the vascular wall as integrative phenomenon.

pound pathobiologic profile that is individually determined by constituent components of the vascular wall affected. Macrophages are exquisitely sensitive to their microenvironment,

Attributes of Hypoxic Preconditioning Determine the Complicating Atherogenesis of Plaques

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

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It is therefore in terms of quantitative realization that atherogenesis is both initiating and progressive influence in the determination of profile progression of the individual athero‐

Foam cells are pivotal in inducing a series of chemotactic phenomena in atherogenesis in a manner that contributes to the self-progressive nature of the disease process. In terms of dis‐ tributional injury, the paramount characterization of the processes in atherosclerosis is fo‐ cused clinically in the emergence of the complicated atherosclerotic plaque. In such a setting, the contributions by procoagulation of the disturbed blood flow prove a central

Attributing significant paramount dynamics in atherogenesis to a series of events of accu‐ mulative effect of oxidized lipoprotein is a characterization in the establishment of self-pro‐ motional progression within any individual atherosclerotic lesion. It is the realization of quantitative identification of such individual plaques that allows for the emergence of sys‐

Chronic inflammation is implicated in atherogenesis with cytokine involvement in all stages

The distributional dynamics of promotional events are primarily permissive in a mode of further contributing influence in atherogenesis. Hypoxia-inducible factor-1 initiates forma‐ tion of foam cells, endothelial cell dysfunction, apoptosis angiogenesis and progressive in‐

It is only in terms of a systemic event that integrates as the individual atherosclerotic plaque that one can realize a transformation of a primarily accumulative lesion to the complicated

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‐

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

butions for further different forms of injury to other components of the vascular wall.

player in the determination of stenosis as predisposition to plaque rupture.

influencing plaque rupture and thrombosis [40].

temic effect within much of the vascular arterial tree.

of plaque development [3].

flammation [10].

atherosclerotic plaque.

**8. Tunica intima**

sclerotic plaque.

**7. Foam cells**

The realization of oxidized lipoproteins may well prove a central participant in the orches‐ tration of events inducing injury as a self-progressive culmination in atherogenesis and in further progression of individual atherosclerotic plaques. Identification of pathway events that distribute the lesions within systems of a primarily promotional nature indicates that macrophages and foam cells promote atherogenesis as a primarily distributional series of quantitative nature. Epigenetic modification of the genome may link environmental injury to gene regulation [41]. Apoptosis and suppressed clearance of apoptotic macrophages ren‐ der plaques susceptible to rupture, promoting thrombosis [13].
