**4. Injury**

Distributional patterns of lesion infliction correlate also with procoagulant effects that system‐ ically compromise recoverability from injury to various components of the vascular wall.

Patterned autonomy of lesion creation and of progression contrasts with a realization of pro‐ moted endothelial dysfunction in terms of quantitative dimensions. Lipids in atherosclerotic lesions weaken cellular antioxidant action through generation of H2O and promote plaque progression [33]. Lipoprotein plays a role in inducing endothelial dysfunction [32]. It is criti‐ cally significant to view the distribution of lesions that arise as hemodynamic forces of lami‐ nar flow on the one hand and as disturbed dynamics of flow at vascular branch points.

The further participation of pathways of identifiable injury arise from a realization of ongo‐ ing progression of individual lesions that conform to tunica intimal targeting in lipoprotein deposition. Apolipoprotein E4 causes macrophage dysfunction and enhances apoptosis by inducing ER stress; it is a major genetic risk factor in atherosclerosis and diabetes [2].

The various component remodellings within the vascular intima are paramount considera‐ tion in the realization of an injury that goes beyond the concept of a primary endothelial form of injury. In such manner, the roles played by oxidized lipoproteins are central to a wide distributional series of patterns that are distinguished primarily by their quantitative attributes. Inflammation and metabolism are important drivers of atherogenesis in the con‐

Primary disorders such as diabetes mellitus, hypertension, and abnormal homocysteine me‐ tabolism are examples of promoting pathways that contribute in the identification of sus‐ ceptibility patterns of non-resolution of emerging atherosclerotic lesions in various loci within the arterial vascular tree. In such manner, compounding influences of highly hetero‐ geneous nature constitute a specific marker in the pathogenesis of atherosclerosis. Inflam‐ mation and immunity in the "infection hypothesis" may form a biologic substrate for atherogenesis [28]. Fibroblast growth factor receptor 4 is implicated in vascular smooth mus‐

Significant performance of injurious agonists allow for permissive emergence of dysfunc‐ tional endothelial cells in a mode of participation that includes a shift especially of pheno‐ typic determination of such vascular wall components as smooth muscle cells from the tunica media. Within such a setting, the distributional attributes of a contractile versus se‐ cretory phenotype of smooth muscle cells allows for the expression of injurious agonists that further compromise the recoverability from endothelial cell injury in particular. The func‐ tion of the ubiquitin-proteasome system deviates from the norm in atherogenesis and this

**2. Patterned autonomy**

238 Current Trends in Atherogenesis

text of HIV infection [18].

**3. Agonists**

cle cell proliferation and atherosclerosis [5].

The systems of promotional realization of injury as induced by atherosclerotic plaques are a significant compound system that incriminates adhesion of monocytes to dysfunctional or activated endothelium.

The participation of injury to the arterial wall is complex and acts as a series of overlapping influences that further contributes to injury as evidenced by the action of evolving hypoxic influence and by procoagulant activity. Almost all coagulant proteins including tissue factor are found in atherosclerotic plaques [19]. Low matrix metalloproteinase-2 levels correlate with intra-cranial location of atherosclerosis [15].

The overlapping series of dynamic events in atherogenesis is permissive in promoting a pathway realization that is central to hypoxia inducing further progression of the lesions. High glycemic load glycemic index are related to significantly increased risk for atherogene‐ sis in women in particular [20].
