Lysyl oxidase expression in smooth muscle cells determines the level of intima calcification in hypercholesterolemia-induced atherosclerosis

Ballester-Servera, Carme; Alonso, Judith; Taurón, Manel; Rotllán, Noemí; Rodríguez, Cristina; Martínez-González, José

doi:10.1016/j.artere.2024.09.001

Clínica e Investigación en Arteriosclerosis (English Edition)

2024

DOI: 10.1016/j.artere.2024.09.001

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Lysyl oxidase expression in smooth muscle cells determines the level of intima calcification in hypercholesterolemia-induced atherosclerosis

Carme Ballester-Servera,

Judith Alonso,

Manel Taurón

et al.

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2024

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Lysyl Oxidase in Ectopic Cardiovascular Calcification: Role of Oxidative Stress

Ballester-Servera,

Alonso,

Cañes

et al. 2024

Antioxidants

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Lysyl oxidase (LOX)-mediated extracellular matrix crosslinking modulates calcification in atherosclerosis and aortic valve disease; however, this enzyme also induces oxidative stress. We addressed the contribution of LOX-dependent oxidative stress to cardiovascular calcification. LOX is upregulated in human-calcified atherosclerotic lesions and atheromas from atherosclerosis-challenged LOX transgenic mice (TgLOXVSMC) and colocalized with a marker of oxidative stress (8-oxo-deoxyguanosine) in vascular smooth muscle cells (VSMCs). Similarly, in calcific aortic valves, high LOX expression was detected in valvular interstitial cells (VICs) positive for 8-oxo-deoxyguanosine, while LOX and LOXL2 expression correlated with osteogenic markers (SPP1 and RUNX2) and NOX2. In human VICs, mito-TEMPO and TEMPOL attenuated the increase in superoxide anion levels and the mineralization induced by osteogenic media (OM). Likewise, in OM-exposed VICs, β-aminopropionitrile (a LOX inhibitor) ameliorated both oxidative stress and calcification. Gain- and loss-of-function approaches in VICs demonstrated that while LOX silencing negatively modulates oxidative stress and calcification induced by OM, lentiviral LOX overexpression exacerbated oxidative stress and VIC calcification, effects that were prevented by mito-TEMPO, TEMPOL, and β-aminopropionitrile. Our data indicate that LOX-induced oxidative stress participates in the procalcifying effects of LOX activity in ectopic cardiovascular calcification, and highlight the multifaceted role played by LOX isoenzymes in cardiovascular diseases.

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Lysyl Oxidase in Ectopic Cardiovascular Calcification: Role of Oxidative Stress

Ballester-Servera,

Alonso,

Cañes

et al. 2024

Antioxidants

View full text Add to dashboard Cite

show abstract

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Lysyl oxidase expression in smooth muscle cells determines the level of intima calcification in hypercholesterolemia-induced atherosclerosis

Cited by 1 publication

References 37 publications

Lysyl Oxidase in Ectopic Cardiovascular Calcification: Role of Oxidative Stress

Lysyl Oxidase in Ectopic Cardiovascular Calcification: Role of Oxidative Stress

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