{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,4]],"date-time":"2026-11-04T20:37:20Z","timestamp":1793824640950,"version":"4.6.1"},"reference-count":38,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"6628","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Science"],"published-print":{"date-parts":[[2023,1,13]]},"abstract":"<jats:p>\n                    CRISPR-Cas9 gene editing is emerging as a prospective therapy for genomic mutations. However, current editing approaches are directed primarily toward relatively small cohorts of patients with specific mutations. Here, we describe a cardioprotective strategy potentially applicable to a broad range of patients with heart disease. We used base editing to ablate the oxidative activation sites of CaMKII\u03b4, a primary driver of cardiac disease. We show in cardiomyocytes derived from human induced pluripotent stem cells that editing the\n                    <jats:italic>CaMKII\u03b4<\/jats:italic>\n                    gene to eliminate oxidation-sensitive methionine residues confers protection from ischemia\/reperfusion (IR) injury. Moreover,\n                    <jats:italic>CaMKII\u03b4<\/jats:italic>\n                    editing in mice at the time of IR enables the heart to recover function from otherwise severe damage.\n                    <jats:italic>CaMKII\u03b4<\/jats:italic>\n                    gene editing may thus represent a permanent and advanced strategy for heart disease therapy.\n                  <\/jats:p>","DOI":"10.1126\/science.ade1105","type":"journal-article","created":{"date-parts":[[2023,1,12]],"date-time":"2023-01-12T13:57:43Z","timestamp":1673531863000},"page":"179-185","update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":124,"title":["Ablation of CaMKII\u03b4 oxidation by CRISPR-Cas9 base editing as a therapy for cardiac disease"],"prefix":"10.1126","volume":"379","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4525-797X","authenticated-orcid":true,"given":"Simon","family":"Lebek","sequence":"first","affiliation":[{"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA."},{"name":"Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA."},{"name":"Department of Internal Medicine II, University Hospital Regensburg, 93053 Regensburg, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3877-527X","authenticated-orcid":true,"given":"Francesco","family":"Chemello","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA."},{"name":"Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, 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