ReviewJournal of cellular and molecular medicine2026
Lipoprotein(a), Endothelial Dysfunction and Cardiovascular Disease.
Review in Journal of cellular and molecular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Lipoprotein(a) (Lp(a)) is a particle similar to low-density lipoprotein cholesterol and is associated with apolipoprotein (A). High Lp(a) levels are a genetic, independent risk factor for atherosclerotic cardiovascular disease (ASCVD). Endothelial cells, which form the continuous lining of the cardiovascular system, are crucial for vascular function and represent the primary target of Lp(a)-mediated injury. Lp(a) penetrates the endothelial barrier and undergoes oxidative modification, triggering endothelial dysfunction, which is characterized by inflammation, oxidative stress and impaired nitric oxide bioavailability. These disruptions promote monocyte recruitment, foam cell formation and atherosclerosis development. Currently, various drugs that can reduce Lp(a) levels are also involved in regulating endothelial cell function, ultimately reducing the risk of ASCVD. However, the molecular mechanisms underlying Lp(a)-mediated endothelial injury and the extent to which Lp(a) lowering improves endothelial function remain incompletely defined. Clarifying these issues may inform cardiovascular risk stratification and the clinical development of Lp(a)-targeted therapies. This review seeks to consolidate the understanding of the link between Lp(a) levels and endothelial dysfunction, highlighting its pivotal role in cardiovascular disease progression.
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Registered trials
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