ArticleArteriosclerosis, thrombosis, and vascular biology2026
Lipoprotein(a) and Vascular Redox State in Patients With Advanced Coronary Atherosclerosis.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed.
- Lipoprotein(a) in Essential Hypertension: Associations with Blood Pressure and Hypertension-Mediated Organ Damage.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2026Observational
- Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target.Cells · 2026Review
- Lipoprotein(a) and the Vascular Redox Interface: Linking Arteriosclerosis, Thrombosis, and Vascular Biology.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
Corrections and comments
- Commented on by
Authors and funding
21 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLp(a) (lipoprotein[a]) is associated with cardiovascular disease, but neither the causal nature nor the underlying mechanisms are fully documented. This study investigated whether Lp(a) triggers atherogenesis by dysregulating vascular redox-sensitive inflammatory state.
methodsPlasma Lp(a) was measured in 1027 patients with advanced coronary artery disease undergoing cardiac surgery. These patients were genotyped, and a modified
resultsIncreased plasma Lp(a) (
conclusionsThis study demonstrates for the first time that a genetically determined increase in plasma Lp(a) results in dysregulated vascular redox/nitrosative signaling in patients with atherosclerosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.