Role of Lipoprotein(a) in Aortic Valve Calcification: Inflammatory and Oxidative Mechanisms Involved.
A, P.B., C, R.M., D, R.B., J, S.R., V, R.O., C, L.J., V, B.M., C, B.S., A, M.A., & T, H.C. (2026). Role of Lipoprotein(a) in Aortic Valve Calcification: Inflammatory and Oxidative Mechanisms Involved.. International journal of molecular sciences. https://doi.org/10.3390/ijms27156639
A PB, C RM, D RB, J SR, V RO, C LJ, et al. Role of Lipoprotein(a) in Aortic Valve Calcification: Inflammatory and Oxidative Mechanisms Involved.. International journal of molecular sciences. 2026; doi: 10.3390/ijms27156639
A PB, C RM, D RB, et al. Role of Lipoprotein(a) in Aortic Valve Calcification: Inflammatory and Oxidative Mechanisms Involved.[J]. International journal of molecular sciences. 2026. DOI: 10.3390/ijms27156639.
@article{a2026,
author = {Polo-Barranco A and Rebolledo-Maldonado C and Rodelo-Barrios D and Solano-Ropero J and Rada-Obeso V and Lavalle-Jiménez C and Blanchar-Martínez V and Beltran-Sánchez C and Maza-Arnedo A and Herrera-Calvo T},
title = {Role of Lipoprotein(a) in Aortic Valve Calcification: Inflammatory and Oxidative Mechanisms Involved.},
journal = {International journal of molecular sciences},
year = {2026},
doi = {10.3390/ijms27156639},
note = {PMID: 42589297},
}
TY - JOUR AU - Polo-Barranco A AU - Rebolledo-Maldonado C AU - Rodelo-Barrios D AU - Solano-Ropero J AU - Rada-Obeso V AU - Lavalle-Jiménez C AU - Blanchar-Martínez V AU - Beltran-Sánchez C AU - Maza-Arnedo A AU - Herrera-Calvo T TI - Role of Lipoprotein(a) in Aortic Valve Calcification: Inflammatory and Oxidative Mechanisms Involved. T2 - International journal of molecular sciences PY - 2026 DO - 10.3390/ijms27156639 AN - PMID:42589297 ER -
Elevated plasma lipoprotein(a) [Lp(a)] levels represent a predominantly genetically determined risk factor for atherosclerotic cardiovascular disease and calcific aortic valve disease (CAVD). Mechanistically, Lp(a) transports oxidized phospholipids, lysophosphatidylcholine, and autotaxin, components capable of promoting inflammation, oxidative stress, and valvular fibrocalcific remodeling. This review synthesizes the molecular, cellular, and clinical evidence linking Lp(a) to CAVD progression. Retention of Lp(a) and other apolipoprotein B-containing lipoproteins in the valvular matrix promotes endothelial activation, recruitment of cells of the monocytic lineage, and the release of proinflammatory mediators. Oxidized phospholipids and the autotaxin-lysophosphatidic acid axis activate redox-dependent pathways and promote the transition of valvular interstitial cells toward myofibroblastic and/or osteogenic phenotypes. These processes converge in alterations in cholesterol metabolism, the release of procalcifying extracellular vesicles, and hydroxyapatite nucleation. Genetic and imaging evidence supports an association between elevated Lp(a), microcalcifying activity, and accelerated hemodynamic progression. Although anti-Lp(a) therapies substantially reduce plasma Lp(a) concentrations, their effect on valvular outcomes has not yet been demonstrated.