
Whole-exome sequencing of early-onset coronary atherosclerotic disease (EOCAD) patients without conventional risk factors identified six potential susceptibility genes: CABP1, HLA-E, TOE1, HPSE2, CHST14, and KLHL8. Variants in these genes were linked to dyslipidemia and inflammatory pathways. Mutation carriers showed elevated LDL cholesterol levels, altered neutrophil and monocyte proportions, and increased residual inflammatory risks. These findings advance precision prevention for EOCAD.
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