**2. Patterned autonomy**

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‐ text of HIV infection [18].

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‐ cle cell proliferation and atherosclerosis [5].
