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This study aims to evaluate the association between\n                    <jats:italic>ACE<\/jats:italic>\n                    insertion\/deletion (I\/D) and\n                    <jats:italic>AGTR1<\/jats:italic>\n                    rs5186A\u2009&gt;\u2009C variants with the occurrence and progression of ROP in a Polish cohort. A total of 377 premature infants were enrolled in the study. The\n                    <jats:italic>ACE<\/jats:italic>\n                    variant was evaluated using PCR, and\n                    <jats:italic>AGTR1<\/jats:italic>\n                    was assessed using TaqMan probes. Clinical characteristics, including risk factors and comorbidities, were documented. A meta-analysis of the effects of the studied variants on ROP was also conducted. The\n                    <jats:italic>AGTR1<\/jats:italic>\n                    rs5186C allele was significantly associated with both the progression of ROP and treatment outcomes. Homozygotes exhibited a 2.47-fold increased risk of developing proliferative ROP and a 4.82-fold increased risk of treatment failure. The impact of this allele increased at low birth weight. A meta-analysis, including 191 cases and 1661 controls, indicated an overall risk of 1.7 (95%CI 1.02\u20132.84) for the recessive effect of the rs5186C allele. The\n                    <jats:italic>ACE<\/jats:italic>\n                    variant did not show a significant association with ROP in our population; however, a meta-analysis of 996 cases and 2787 controls suggested a recessive effect of the insertion allele (an odds ratio of 1.21 (95%CI 1.00\u20131.60)). These results indicate that gain-of-function\n                    <jats:italic>AGTR1<\/jats:italic>\n                    variants may play a crucial role in the development of ROP, potentially by promoting angiogenesis and pro-inflammatory effects. Screening for these variants could facilitate the development of personalized risk assessment and treatment strategies for ROP.\n                  <\/jats:p>","DOI":"10.1007\/s13353-024-00900-0","type":"journal-article","created":{"date-parts":[[2024,8,26]],"date-time":"2024-08-26T00:02:30Z","timestamp":1724630550000},"page":"911-923","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Association of ACE and AGTR1 variants with retinopathy of prematurity: a case\u2013control study and meta-analysis"],"prefix":"10.1007","volume":"66","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6966-6885","authenticated-orcid":false,"given":"Anna","family":"Durska","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dawid","family":"Szpecht","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3790-4583","authenticated-orcid":false,"given":"Anna","family":"Gotz-Wi\u0119ckowska","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8275-3126","authenticated-orcid":false,"given":"Ewa","family":"Strauss","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2024,8,26]]},"reference":[{"issue":"5","key":"900_CR1","doi-asserted-by":"publisher","first-page":"1858","DOI":"10.1542\/peds.2006-1088","volume":"118","author":"MJ Bizzarro","year":"2006","unstructured":"Bizzarro MJ, Hussain N, Jonsson B, Feng R, Ment LR, Gruen JR, Zhang H, Bhandari V (2006) Genetic susceptibility to retinopathy of prematurity. 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