Potential mechanisms linking oxidized LDL to susceptibility to cancer

Abstract

Last decades have witnessed an explosive growth of obesity in developed countries. This condition is associated with not only increased risk for atherosclerosis and resultant cardiovascular pathologies but also confers significant increase in probability for the development of various forms of cancer. Experimental and epidemiological evidence accumulated in respective fields highlights multiple overlaps in pathobiology of atherosclerosis and cancer including signaling pathways, inflammation, cytokine involvement, proliferation, and angiogenesis. Recent discovery of additional layer of regulation of gene expression based on miRNAs also revealed multiple similarities in miRNA profiles. This suggests that atherogenesis and obesity-mediated increase in susceptibility to cancers may have common etiological roots. Recent advances in cardiovascular research identified oxidatively modified LDL (and not LDL itself) as a primary factor responsible for initiation and progression of atherogenesis, and the analysis of potential involvement of ox-LDL in carcinogenesis is the focus of the present review.