Genome-Wide Scan for Quantitative ACE Activity in Taiwan Young-Onset Hypertension StudyWang R.-Y.a, c · Chung C.-M.b · Fann C.S.J.b · Yang H.-C.d · Chen J.-W.e · Jong Y.-S.f · Jou Y.-S.b · Lo H.-M.f · Ho F.-M.f · Kang C.-S.g · Chen C.-C.h · Chang H.-C.h · Shyue S.-K.b · Pan W.-P.b, i
aGraduate Institute of Life Science, National Defense Medical Center, bInstitute of Biomedical Sciences, Academia Sinica, Taipei, cDepartment of Public Health, China Medical University, Taichung, dInstitute of Statistical Science, Academia Sinica, eDepartment of Cardiology, Taipei Veterans General Hospital, and Cardiovascular Research Center, National Yang-Ming University, Taipei, fDepartment of Cardiology, Tao-Yuan General Hospital Department of Health, and gDepartment of Cardiology, Min-Sheng Hospital, Taoyuan, hDepartment of Cardiology, Lin-Shin Hospital, Chung-Li, iInstitute of Epidemiology, School of Public Health, National Taiwan University, Taipei, Taiwan, ROC
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Objectives: Angiotensin converting enzyme (ACE) plays major roles in the pathogenesis of cardiovascular diseases (CVD). However, findings on the relations between ACEvariants and CVD have not been consistent. The purpose of this study was to map quantitative trait loci (QTL) for serum ACE activity, a heritable endophenotype of cardiovascular diseases (estimated heritability = 0.58). Methods: With 1,271 individuals from 373 young-onset (age ≤40) hypertension pedigrees, 479 deCODE microsatellite markers were genotyped. Results: We identified a previously unknown loci on chromosomes 9 at 149.4 cM (LOD = 3.00) in addition to a strong linkage peak near the ACE structural locus on chromosome 17 at 89.6 cM (LOD = 4.60). Conclusions: These results not only indicate that the ACE gene or nearby loci on 17q was among the strongest QTL influencing ACE activity, but also reveal a potential ACE QTL in human genome, pointing to the complexity of ACE regulation.
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