ReviewCurrent cardiology reports2026
The Implications of Lipoprotein(a) in MASLD.
Review in Current cardiology reports, 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
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewLipoprotein(a) [Lp(a)] remains a well-established, genetically determined predictor of cardiovascular risk due to its pro-atherogenic and pro-thrombotic effects. This review examines the paradoxical relationship between Lp(a) and metabolic dysfunction-associated steatotic liver disease (MASLD), where Lp(a) levels decline with advanced fibrosis despite persistently elevated cardiovascular disease (CVD) risk. RECENT
findingsStudies consistently show an inverse association between Lp(a) and MASLD severity. Evidence suggests that lower Lp(a) levels are a consequence of hepatic dysfunction rather than protective against cardiovascular disease. Additionally, selective hepatic insulin resistance increases VLDL production, diverting apoB100 from Lp(a) assembly, while insulin directly suppresses apolipoprotein(a) synthesis. Genetic variants linked to MASLD may further impair hepatic lipid secretion and reduce Lp(a). Lower Lp(a) levels in MASLD likely reflect impaired hepatic synthetic function rather than reduced cardiovascular risk. Recognizing this paradox may improve risk stratification and interpretation of Lp(a) in patients with MASLD.
Indexed as
Identifiers
42570162What 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.