Key result
Novel 5q33.3 variants modulate HAVCR1 expression, linking lipid metabolism directly to inflammation.
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This study establishes a mechanistic link between lipid metabolism and inflammation by identifying HAVCR1 as a key genetic regulator of hyperlipidemia at the 5q33.3 locus.
Hyperlipidemia is a major risk factor for atherosclerosis and other serious cardiovascular diseases, yet it often presents without obvious symptoms in the absence of comorbidities, complicating early detection and management. Given the high heritability of lipid traits, genome-wide association studies (GWAS) have identified numerous loci associated with serum lipids; however, pinpointing the causal variants remains a challenge. Here, we investigated the 5q33.3 locus and identified HAVCR1 as a likely effector gene influencing lipid metabolism. By integrating functional genomics and experimental validation, we identified two non-linked variants, rs6882076 and rs17573010, that modulate HAVCR1 via allele-specific binding by IRF2 and GATA4, respectively. rs6882076 was refined from prior GWAS findings, while rs17573010 emerged from ancestry-specific analysis. These findings highlight the complexity of genetic regulation across populations and establishes a mechanistic link between lipid metabolism and inflammation, offering insights into the genetic basis of hyperlipidemia and its potential translational relevance.
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Chen et al. (2026) studied Hyperlipidemia. 5q33.3 locus variants (rs6882076 and rs17573010) was evaluated on HAVCR1 modulation and lipid metabolism. Functional genomic analysis identified two variants, rs6882076 and rs17573010, at the 5q33.3 locus that modulate HAVCR1 via allele-specific binding, linking lipid metabolism and inflammation.
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