{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T01:58:43Z","timestamp":1777859923343,"version":"3.51.4"},"reference-count":32,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2010,12,16]],"date-time":"2010-12-16T00:00:00Z","timestamp":1292457600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2011,9]]},"abstract":"<jats:p>\n                    Introduction. Hypertrophic cardiomyopathy (HCM), an inherited primary cardiac disorder mostly caused by defective sarcomeric proteins, serves as a model to investigate left ventricular hypertrophy (LVH). HCM manifests extreme variability in the degree and distribution of LVH, even in patients with the same causal mutation. Genes coding for renin\u2014angiotensin\u2014aldosterone system components have been studied as hypertrophy modifiers in HCM, with emphasis on the angiotensin (Ang) II type 1 receptor (AT\n                    <jats:sub>1<\/jats:sub>\n                    R). However, Ang II binding to Ang II type 2 receptors (AT\n                    <jats:sub>2<\/jats:sub>\n                    R) also has hypertrophy-modulating effects.\n                  <\/jats:p>\n                  <jats:p>\n                    Methods. We investigated the effect of the functional +1675 G\/A polymorphism (rs1403543) and additional single nucleotide polymorphisms in the 3\u2019 untranslated region of the AT\n                    <jats:sub>2<\/jats:sub>\n                    R gene ( AGTR2) on a heritable composite hypertrophy score in an HCM family cohort in which HCM founder mutations segregate.\n                  <\/jats:p>\n                  <jats:p>Results. We find significant association between rs1403543 and hypertrophy, with each A allele decreasing the average wall thickness by ~0.5 mm, independent of the effects of the primary HCM causal mutation, blood pressure and other hypertrophy covariates ( p = 0.020).<\/jats:p>\n                  <jats:p>\n                    Conclusion. This study therefore confirms a hypertrophy-modulating effect for AT\n                    <jats:sub>2<\/jats:sub>\n                    R also in HCM and implies that +1675 G\/A could potentially be used in a panel of markers that profile a genetic predisposition to LVH in HCM.\n                  <\/jats:p>","DOI":"10.1177\/1470320310390725","type":"journal-article","created":{"date-parts":[[2010,12,16]],"date-time":"2010-12-16T21:05:36Z","timestamp":1292533536000},"page":"274-280","source":"Crossref","is-referenced-by-count":12,"title":["Genetic variation in angiotensin II type 2 receptor gene influences extent of left ventricular hypertrophy in hypertrophic cardiomyopathy independent of blood pressure"],"prefix":"10.1177","volume":"12","author":[{"given":"Nadia","family":"Carstens","sequence":"first","affiliation":[{"name":"MRC Centre for Molecular and Cellular Biology, Department of Biomedical Sciences, University of Stellenbosch Health Sciences Faculty, Tygerberg, South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lize","family":"van der Merwe","sequence":"additional","affiliation":[{"name":"Biostatistics Unit, Medical Research Council of South Africa, Tygerberg, South Africa, Department of Statistics, University of Western Cape, Bellville, South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Miriam","family":"Revera","sequence":"additional","affiliation":[{"name":"Department of Cardiology, IRCCS San Matteo Hospital, Pavia, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marshall","family":"Heradien","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Stellenbosch Health Sciences Faculty, Tygerberg, South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Althea","family":"Goosen","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Stellenbosch Health Sciences Faculty, Tygerberg, South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul A","family":"Brink","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Stellenbosch Health Sciences Faculty, Tygerberg, South Africa"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Johanna C","family":"Moolman-Smook","sequence":"additional","affiliation":[{"name":"MRC Centre for Molecular and Cellular Biology, Department of Biomedical Sciences, University of Stellenbosch Health Sciences Faculty, Tygerberg, South Africa,"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2010,12,16]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/4.suppl_1.1721"},{"key":"atypb2","doi-asserted-by":"crossref","first-page":"104","DOI":"10.1111\/j.1540-8167.2007.00965.x","volume":"19","author":"Alcalai R.","year":"2008","journal-title":"J Cardiovasc 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