ArticleCardiovascular diabetology2025
Interplay among lipoprotein(a), hepatic and vascular damage in individuals with metabolic dysfunction.
Article in Cardiovascular diabetology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Heart-liver co-management in MASLD: expert perspectives and recommendations from a multidisciplinary cardiometabolic framework.Nature reviews. Gastroenterology & hepatology · 2026Review
- Lipoprotein(a), insulin resistance, and cardiovascular outcomes in metabolic dysfunction-associated steatotic liver disease.Cardiovascular diabetology · 2026Article
- Sex- and menopause-specific inverse associations between metabolic dysfunction-associated steatotic liver disease and serum lipoprotein(a) concentrations: evidence from SHIP and UK Biobank.Cardiovascular diabetology · 2026Article
- Prevalence of Elevated Lipoprotein(a) and Its Association with Cardiovascular Disease in Patients with Overweight and Obesity in Argentina.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
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Authors and funding
20 authors.
Funding
Abstract
backgroundThe relationship between plasma lipoprotein(a) [Lp(a)] levels and metabolic dysfunction-associated steatotic liver disease (MASLD) remains unclear. The aim of this study was to examine the combined effects of Lp(a) levels on liver and vascular damage.
methodsThe study was conducted using the Liver-Bible cohort of individuals with metabolic dysfunction (n = 859, 808 with genomic information) and the Milan Biobank (n = 6963). Genome-wide association studies (GWAS) and polygenic risk scores (PRS) were used to evaluate the inherited factors influencing plasma Lp(a) levels.
resultsIn the Liver-Bible cohort, genetic variation in the LPA gene was the strongest determinant of Lp(a), followed by liver stiffness measurement (LSM). Additionally, circulating Lp(a) levels, but not genetic predisposition, were inversely related to LSM, suggesting that MASLD severity may affect Lp(a) secretion. Among participants with more severe insulin resistance (n = 250), Lp(a) levels (odds ratio 6.7, 95% CI 1.0-53.0, p = 0.046) and LSM (odds ratio 13.7, 95% CI 1.4-172.2, p = 0.023) were associated with greater prevalence of carotid atherosclerotic plaques, regardless of traditional cardiovascular risk factors. In the Milan Biobank, genetically predicted higher Lp(a) levels tended to increase the risk of liver-related outcomes, whereas genetically predicted MASLD was associated with lower circulating Lp(a) levels.
conclusionsThe results of this study suggest that liver damage is more likely the cause of reduced plasma Lp(a) levels rather than a consequence. Assessing plasma Lp(a) levels and the extent of liver damage could improve the prediction of vascular damage.
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