{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T01:57:34Z","timestamp":1777859854000,"version":"3.51.4"},"reference-count":34,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2014,3,3]],"date-time":"2014-03-03T00:00:00Z","timestamp":1393804800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2015,9]]},"abstract":"<jats:sec>\n                    <jats:title>Background and objective:<\/jats:title>\n                    <jats:p>The cornerstone of dermatomyositis (DM) pathogenesis involves vascular disturbance that leads to hypoxia, capillary necrosis and muscle perifascicular atrophy. Hence, the hypothesis is that the angiotensin-converting enzyme (ACE) insertion\/deletion (I\/D) gene polymorphism could be associated with susceptibility to DM.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method:<\/jats:title>\n                    <jats:p>A single centre, case control study that genotyped ACE gene in 88 DM and 99 healthy individuals. The ACE gene polymorphism was determined by melting curve analysis of real-time polymerase chain reaction products using SYBR Green.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>The DM and the control subjects had a comparable mean age, gender frequency and ethnicity. The frequency of the D allele was higher in DM than in the control individuals (63.6% vs 55.6%, respectively). The DM had more ACE D\/D and less ACE I\/D genotype when compared to the control individuals, whereas the ACE I\/I genotype distribution was similar in both case and control groups. Moreover, after sex-age-adjusted analysis, the ACE D\/D genotype was strongly associated with DM disease (odds ratio (OR) 2.44, 95% confidence interval (CI): 1.17\u20134.37), in contrast to ACE I\/D genotype (OR 0.51, 95% CI: 0.28\u20130.93).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>Homozygous ACE D\/D was associated significantly with the DM risk. Further investigations are required to clarify and to confirm the association of these genes with DM susceptibility.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1470320314524995","type":"journal-article","created":{"date-parts":[[2014,3,4]],"date-time":"2014-03-04T00:01:49Z","timestamp":1393891309000},"page":"666-671","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":4,"title":["Angiotensin-converting enzyme insertion\/deletion gene polymorphism is associated with dermatomyositis"],"prefix":"10.1177","volume":"16","author":[{"given":"Samuel K","family":"Shinjo","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Universidade de S\u00e3o Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miyuki","family":"Uno","sequence":"additional","affiliation":[{"name":"Department of Neurology, Universidade de S\u00e3o Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sueli M","family":"Oba-Shinjo","sequence":"additional","affiliation":[{"name":"Department of Neurology, Universidade de S\u00e3o Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Suely KN","family":"Marie","sequence":"additional","affiliation":[{"name":"Department of Neurology, Universidade de S\u00e3o Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2014,3,3]]},"reference":[{"key":"bibr1-1470320314524995","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(03)14368-1"},{"key":"bibr2-1470320314524995","doi-asserted-by":"publisher","DOI":"10.1016\/j.coph.2010.03.001"},{"key":"bibr3-1470320314524995","doi-asserted-by":"publisher","DOI":"10.1016\/0008-8749(87)90278-4"},{"key":"bibr4-1470320314524995","first-page":"33","volume":"117","author":"Alhenc-Gelas F","year":"1991","journal-title":"J Lab Clin 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