Lipids & metabolic liver disease

Multi-omics uncovers the pleiotropic genetic mechanisms linking MASLD and cardiometabolic syndromes

Cardiovasc DiabetolPublished Genome-wide cross-trait analysis with multi-omics integration

Authors' conclusion

This study provides a comprehensive map of the shared genetic architecture between MASLD and CKM syndrome, reveals novel causal genes and repurposable drug targets, and offers insights into precision medicine approaches for cardiometabolic and liver diseases.

Study context

Population
GWAS summary statistics for MASLD and 38 cardiovascular-kidney-metabolic (CKM) traits
Outcome
Shared genetic architecture of MASLD and CKM traits
Methodological detailsGWAS summary statistics, genetic correlation, causal inference, druggability evaluation
  • GWAS summary statistics
  • Genetic correlation
  • Causal inference
  • Druggability evaluation

Main finding

As reported in the abstract

CKM traits with significant genetic correlation with MASLD, especially metabolic and cardiovascular conditions
16
Pleiotropic loci
116
Shared causal variants (e.g. rs429358 near APOE, influencing multiple traits)
65
Unique candidate pleiotropic genes, enriched in lipid and cholesterol metabolism, highly expressed in liver, adipose and immune-related cell types (macrophages, endothelial cells)
152
Genes validated by eQTL and pQTL data from multiple tissues and cohorts
131

Original publication

Multi-omics uncovers the pleiotropic genetic mechanisms linking MASLD and cardiometabolic syndromes. Cardiovasc Diabetol. Published 9 May 2026. doi:10.1186/s12933-026-03180-6

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