{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T02:17:15Z","timestamp":1780453035592,"version":"3.54.1"},"reference-count":73,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,9,16]],"date-time":"2025-09-16T00:00:00Z","timestamp":1757980800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Stimulated by retinoic acid gene 6 (STRA6) is a cell surface receptor that regulates cellular uptake of vitamin A metabolites and cardiac development. We hypothesized that <jats:italic>Stra6<\/jats:italic> expression attenuates ischemic injury-induced heart failure following myocardial infarction (MI) by vitamin A-dependent mechanisms.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>MI was induced in mice with <jats:italic>Stra6<\/jats:italic> germline deletion, vitamin A deficiency (VitAD) by combined <jats:italic>lecithin-retinol acyltransferase (Lrat)<\/jats:italic> germline deletion and feeding with a vitamin A-deficient diet. Contractile function was determined by transthoracic echocardiography, cardiac structure was assessed by histological analysis, and gene profiling was performed by RNA sequencing.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:italic>Stra6<\/jats:italic> deletion and VitAD did not impact contractile function and cardiac structure under basal conditions. <jats:italic>Stra6<\/jats:italic> deficiency resulted in myocardial rupture, with the majority of mice dying by 4 days post-MI, which additional VitAD attenuated. Interestingly, contractile function, mRNA expression of heart failure markers, and cardiac structure were not different between groups 3 days post-MI. Gene profiling 3 days post-MI revealed decreased Wnt signaling in <jats:italic>Stra6<\/jats:italic>-deficient relative to wildtype hearts, which was reversed by VitAD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The present study identifies an unexpected role for VitAD, which preserves Wnt signaling and attenuates cardiac rupture in <jats:italic>Stra6<\/jats:italic>-deficient hearts following ischemic injury.<\/jats:p><\/jats:sec>","DOI":"10.3389\/fcvm.2025.1626769","type":"journal-article","created":{"date-parts":[[2025,9,16]],"date-time":"2025-09-16T05:34:29Z","timestamp":1758000869000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Vitamin A deficiency attenuates cardiac rupture in Stra6-deficient hearts following ischemic 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