ArticleEuropean heart journal open2025
Fuelling aortic stenosis: the integral role of 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3-mediated glycolysis in Lp(a)-induced valve inflammation.
Article in European heart journal open, 2025. 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) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target.Cells · 2026Review
- Lipoprotein(a) and Aortic Stenosis: From Genetic Risk to Emerging Therapeutic Strategies.European cardiology · 2026Review
- Glycolysis hijacked: a novel pathogenic role of lipoprotein(a) in valve disease.European heart journal open · 2025Article
Corrections and comments
- Comment on
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: Calcific aortic valve disease is the most common valvular heart disease characterized by an inflammatory response in the leaflets followed by fibro-calcific remodelling of valvular interstitial cells (VICs). Lipoprotein(a) [Lp(a)] is a well-recognized risk factor for CAVD, however the role of metabolism in driving Lp(a)-induced inflammation remains largely elusive. Therefore, we aim to investigate the role of Lp(a) in driving inflammatory and metabolic changes in VICs and examine how alterations in cellular metabolism can alter their inflammatory phenotype. Methods and results: Inflammatory activity in the aortic valve of patients with mild to severe aortic stenosis with elevated Lp(a) levels (>50 mg/dL) is increased, as reflected by increased Conclusion: Lipoprotein(a)-induced PFKFB3-mediated glycolysis in VICs sustains NF-κB-dependent inflammatory response. These insights into the inflammation-metabolic axis may offer a more refined approach to decrease valvular inflammation.
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.