**7. Foam cells**

endothelium is a prototype example of distributional nature in denoting a systemic partici‐ pation of further ongoing transformation in phenotype characterization of cellular compo‐

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‐

The complicated atherosclerotic plaque is thus a series of overlying pathways of influence that concurrently participate in identifying the different component systems in pathogene‐ sis. Regulating T cells and serum interleukin-10 may exert a protective role against plaque rupture in patients with coronary atherosclerosis [11]. It is with contextual reference to oxi‐ dized lipoprotein deposits within the intima that phenomena of adherence to dysfunctional endothelium induce leukocytes as systemic agonists in atherogenesis. The role of platelets in

The sharp distinction in identification of progression of an individual plaque from the rup‐ tured plaque permits the emergence of multiple profiles in developmental history of lesions that individually evolve but that are systemically compounding and overlapping in profile determination. NF-E2 related factor 2 pathway restores redox homeostasis and Nrf2 cross

The realization of injury to endothelial cells is therefore only an initial event in the once-real‐

The dynamics of orchestration of various injurious agonists thus emerge as an essential component system in atherogenesis in a manner that calls into operative participation multi‐ ple heterogeneous pathways ranging from procoagulant effect of disturbed blood flow, hy‐ poxia, dysfunctional reduction in nitric oxide production and action, and especially the chemotactic influences as induced by oxidized lipoproteins deposited in the intima. Arachi‐ donic acid increases inflammation and enhances the ability of endothelial cells to bind mon‐ ocytes in vivo [12]. The further participation of remodelling of the intima as a result of migration and proliferation of smooth muscle cells is evidence for a series of phenotypic switches that allow permissive injury to multiple cell components and to matrix production

It is within a systemically integrative series of active realizations that atherogenesis proves an integrative expression of component pathways; this paradoxically determines a com‐

ized reactivity to injury to multiple components of the vascular wall.

nents of the vascular wall as integrative phenomenon.

der plaques susceptible to rupture, promoting thrombosis [13].

**6. Complicated plaque**

240 Current Trends in Atherogenesis

atherothrombosis is well established [9].

talks with the proteasome [4].

of proteoglycans.

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

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‐ temic effect within much of the vascular arterial tree.

Chronic inflammation is implicated in atherogenesis with cytokine involvement in all stages of plaque development [3].

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‐ flammation [10].

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 atherosclerotic plaque.
