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Deciphering the Role of Oxidized Lipoproteins in Regulating CAVD Pathobiology

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The deposition of oxidized lipids is a hallmark of calcific aortic valve disease (CAVD)1,2, but its relationship to other CAVD features remains unclear. For example, while proteoglycan (PG) enrichment and oxidized low-density lipoprotein (oxLDL) deposition occur early in CAVD3,4, it is not known whether this is stimulated by PGs encouraging the retention of oxLDL or high levels of circulating oxLDL causing VICs to upregulate PG secretion (or a mixture of both). Similarly, few studies have analyzed the effect of oxLDL on VIC phenotype. Furthermore, the potential for lipid oxidation to influence events taking place in later stages of the disease remains mostly unexplored. We hypothesize that oxLDL deposition plays a role in the regulation of other pathological events in CAVD, such as PG enrichment and valvular angiogenesis.

The results of this study indicate that oxLDL is capable of inducing many of the phenotypic changes associated with CAVD progression. Specifically, these findings suggest that deposition of circulating oxLDL may fuel both pathological extracellular matrix remodeling and angiogenesis in the valve. Deciphering the sequence of pathological events in CAVD will help us to not only better understand disease etiology, but also refine approaches to develop targeted treatments.

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