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Editorial
. 2025 Oct 24;121(12):1809-1811.
doi: 10.1093/cvr/cvaf166.

oxLDL-induced aortic valve inflammation and calcification: opportunities for clinical translation

Yu-Jen Wang  1 , Michael A Matter  1   2 , Christian M Matter  1   2
Affiliations
Editorial

oxLDL-induced aortic valve inflammation and calcification: opportunities for clinical translation

Yu-Jen Wang et al. Cardiovasc Res. .
No abstract available

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Conflict of interest statement

Conflict of interest: C.M.M. has received research grants to the institution from EliLilly, AstraZeneca, Roche, Amgen, Novartis, Novo Nordisk, and MSD, including speaker or consultant fees.

Figures

Figure 1
Figure 1
Dyslipidaemia and inflammation are critical contributors to experimental aortic valve calcification and subsequent stenosis. Currently, no pharmacological therapy is available to delay the progression of aortic valve disease in patients. Previous lipid-lowering trials failed to demonstrate clinical benefit. Jiang et al. now report that oxLDL induces FOXS1 expression in VIC, which suppresses PPARγ activity, impairs cholesterol efflux (via ABCA1/ABCG1), and activates the NLRP3 inflammasome. This novel mechanistic insight prompts a re-evaluation of lipid-lowering strategies in patients with aortic sclerosis up to calcific aortic valve stenosis. In particular, factors such as duration of drug therapy, baseline lipid levels and dosing regimens of lipid-lowering therapies, the targeted lipid species (e.g. LDL-C and Lp(a)), and aortic valve disease stage likely influence the therapeutic effects. oxLDL, oxidized low-density lipoprotein; FOXS1, forkhead box S1; PPARγ, peroxisome proliferator-activated receptor γ; ABCA1, ATP binding cassette subfamily A member 1; ABCG1, ATP-binding cassette subfamily G member 1; NLRP3, nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3; VIC, valvular interstitial cell; CAVD, calcific aortic valve disease; LDL-C, low-density lipoprotein cholesterol; Lp(a), lipoprotein(a).
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Comment on

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