성균관대학교 · Medicine
홍희원 교수의 연구실은 심혈관질환과 대사질환의 유전적 기반을 밝히는 데 초점을 맞추고 있으며, 특히 유전적 요인과 체질량, 직업적 지위 등 생활사슬과의 상관관계를 통합적으로 분석합니다. 대규모 유전체 연관 연구(GWAS)와 에피제놈 데이터를 융합해 질병의 생물학적 메커니즘을 규명하고, 유전적 위험 요소가 심혈관질환에 미치는 영향을 실질적인 예방 전략으로 연결하는 데 기여합니다. 특히, 유전적 위험과 생활습관의 상호작용이 질병 발생에 미치는 영향을 탐구하는 데 주력하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
High adiposity is associated with increased CVD risk despite divergent evidence gradients. Adiposity was a causal risk factor for CVD except all-cause mortality and stroke. Half (49%; 26/53) of the associations were supported by high-level evidence. The associations were consistent between sexes and across global regions. This study provides guidance on how to integrate evidence from observational (association) and genetics-driven (causation) studies accumulated to date, to enable a more reliabl
Large genome-wide association studies (GWAS) have identified many genetic loci associated with risk for myocardial infarction (MI) and coronary artery disease (CAD). Concurrently, efforts such as the National Institutes of Health (NIH) Roadmap Epigenomics Project and the Encyclopedia of DNA Elements (ENCODE) Consortium have provided unprecedented data on functional elements of the human genome. In the present study, we systematically investigate the biological link between genetic variants assoc
Occupational attainment, which represents middle-age cognitive activities, is a known proxy marker of cognitive reserve for Alzheimer's disease. Previous genome-wide association studies have identified numerous genetic variants and revealed the genetic architecture of educational attainment, another marker of cognitive reserve. However, the genetic architecture and heritability for occupational attainment remain elusive. We performed a large-scale genome-wide association study of occupational at
Genetic risk for T2D was associated with increased risks of overall CVD, various CVD subtypes, and fatal CVD. Engaging in a healthy lifestyle and maintaining metabolic health may reduce subsequent risk of CVD regardless of genetic risk for T2D.
