Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors hypothesized that genetic predisposition to diabetes complications would be more evident among low-risk individuals and aimed to identify genes related to developing complications (confirmed distal symmetric polyneuropathy, overt nephropathy, or coronary artery disease) in low-risk groups. Participants in the Pittsburgh, Pennsylvania, Epidemiology of Diabetes Complications Study of childhood-onset type 1 diabetes, first seen in 1986-1988 (mean age, 28 years; diabetes duration, 19 years), were reexamined biennially for 10 years. For each complication, subgroups with the lowest disease risk were identified by using tree-structured survival analysis, and 15 candidate genes were compared between subjects with and without complications. In the group with the lowest incidence of confirmed distal symmetric polyneuropathy (n = 123), confirmed distal symmetric polyneuropathy risk increased fivefold for those with the eNOS GG genotype (p < 0.05). In the group with the lowest risk of overt nephropathy (n = 340), the ACE D polymorphism increased overt nephropathy risk twofold (p = 0.05), whereas a protective effect was observed for the LIPC CC genotype (p < 0.05). In the group with the lowest incidence of coronary artery disease (n = 331), the MTHFR CC genotype increased coronary artery disease risk threefold (p < 0.05). Tree-structured survival analysis may help identify genetic predispositions among individuals who, despite low risk, develop diabetes-related complications.
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PMID:Identifying genetic susceptibilities to diabetes-related complications among individuals at low risk of complications: An application of tree-structured survival analysis. 1692 30

In an electronic search of the literature, the authors systematically retrieved all published studies that investigated genetic susceptibility to peripheral arterial disease (PAD). They created a comprehensive database of all eligible studies, collecting detailed genetic and bioinformatics data on each polymorphism. Data from eligible studies were synthesized using meta-analysis techniques. Gene variants were classified into distinct pathophysiologic pathways, and their potential involvement in PAD pathogenesis was determined. Forty-one publications that examined 44 gene polymorphisms were included. For 37 polymorphisms, the variant form had a functional effect. Twenty-three polymorphisms in 22 potential PAD candidate genes (F2, FGB, MTHFR, ITGB3, ACE, AGT, IL6, CCL2, ICAM1, SELE, MMP9, PPARG, MMP1, ADD1, P2RY12, LIPC, PLA2G7, SCARB1, MMP3, MTTP, LPA, CHRNA3) showed a significant association in individual studies. Eighty-eight percent of the studies had statistical power of less than 50%, and in 15 studies the genotype distribution in the control group did not conform to Hardy-Weinberg equilibrium. Data on 12 polymorphisms (F5 1691 G/A, MTHFR 677C/T, F2 20210 G/A, ITGB3 1565 T/C, ACE I/D, AGT 704C/T, AGT -6G/A, AGT 733C/T, IL6 -174 G/C, MMP9 -1562C/T, ICAM1 1462A/G, CHRNA3 831C/T) were synthesized, and a positive association was found for 3 (IL6 -174 G/C, ICAM1 1462A/G, CHRNA3 831C/T).
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PMID:A field synopsis and meta-analysis of genetic association studies in peripheral arterial disease: The CUMAGAS-PAD database. 1943 65