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Role of Lipoprotein(a) in Aortic Valve Calcification: Inflammatory and Oxidative Mechanisms Involved

Alberto Polo-Barranco1,2, Carlos Rebolledo-Maldonado1,3, Dairo Rodelo-Barrios4,5

  • 1Faculty of Medicine, Universidad Metropolitana de Barranquilla, Barranquilla 080002, Colombia.

International Journal of Molecular Sciences
|August 13, 2026
PubMed

Insights

Elevated lipoprotein(a) [Lp(a)] is a genetic risk factor for calcific aortic valve disease (CAVD). This review details how Lp(a) drives CAVD progression through inflammation and cellular changes.

Area of Science:

  • Cardiovascular Medicine
  • Genetics
  • Biochemistry

Background:

  • Elevated plasma lipoprotein(a) [Lp(a)] is a significant genetically determined risk factor for atherosclerotic cardiovascular disease and calcific aortic valve disease (CAVD).
  • Lp(a) carries oxidized phospholipids, lysophosphatidylcholine, and autotaxin, which contribute to inflammation, oxidative stress, and valvular fibrocalcific remodeling.
  • Understanding the link between Lp(a) and CAVD is crucial for developing targeted therapies.

Purpose of the Study:

  • To synthesize the molecular, cellular, and clinical evidence linking Lp(a) to the progression of CAVD.
  • To elucidate the mechanisms by which Lp(a) contributes to valvular pathology.
  • To review the current understanding of Lp(a)'s role in CAVD.

Main Methods:

  • Review of existing molecular, cellular, and clinical studies.
  • Analysis of the role of Lp(a) in valvular matrix retention and cellular activation.
  • Examination of the impact of oxidized phospholipids and the autotaxin-lysophosphatidic acid axis on valvular cells.
  • Evaluation of genetic and imaging evidence associating Lp(a) with CAVD progression.

Main Results:

  • Lp(a) retention in the valvular matrix promotes endothelial activation, monocyte recruitment, and inflammation.
  • Oxidized phospholipids and the autotaxin-lysophosphatidic acid axis activate redox pathways, driving valvular interstitial cell transformation.
  • These processes lead to altered cholesterol metabolism, procalcifying extracellular vesicle release, and hydroxyapatite nucleation.
  • Genetic and imaging data link elevated Lp(a) to microcalcification and faster hemodynamic progression.

Conclusions:

  • Lp(a) plays a multifaceted role in the pathogenesis of CAVD, involving inflammation, cellular changes, and calcification.
  • While anti-Lp(a) therapies reduce plasma Lp(a) levels, their impact on valvular outcomes requires further investigation.
  • Lp(a) is a key therapeutic target for preventing and treating CAVD.

Keywords:
aortic stenosisautotaxincalcified aortic valve diseasecardiovascular calcificationlipoprotein(a)oxidative stressoxidized phospholipidsvalvular inflammation

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