REFERENCES
1. Lebek S, Chemello F, Caravia XM. Ablation of CaMKIIδ oxidation by CRISPR-Cas9 base editing as a therapy for cardiac disease. Science 2023;379:179-85.
2. Hausenloy DJ, Yellon DM. Myocardial ischemia-reperfusion injury: a neglected therapeutic target. J Clin Invest 2013;123:92-100.
3. He BJ, Joiner ML, Singh MV, et al. Oxidation of CaMKII determines the cardiotoxic effects of aldosterone. Nat Med 2011;17:1610-8.
4. Zhang R, Khoo MS, Wu Y, et al. Calmodulin kinase II inhibition protects against structural heart disease. Nat Med 2005;11:409-17.
5. van Oort RJ, McCauley MD, Dixit SS, et al. Ryanodine receptor phosphorylation by calcium/calmodulin-dependent protein kinase II promotes life-threatening ventricular arrhythmias in mice with heart failure. Circulation 2010;122:2669-79.
6. Zhang T, Maier LS, Dalton ND, et al. The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure. Circ Res 2003;92:912-9.
7. Purohit A, Rokita AG, Guan X, et al. Oxidized Ca2+/calmodulin-dependent protein kinase II triggers atrial fibrillation. Circulation 2013;128:1748-57.
8. Erickson JR, Joiner ML, Guan X, et al. A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation. Cell 2008;133:462-74.
9. Gaudelli NM, Komor AC, Rees HA, et al. Programmable base editing of A•T to G•C in genomic DNA without DNA cleavage. Nature 2017;551:464-71.
10. Anzalone AV, Koblan LW, Liu DR. Genome editing with CRISPR-Cas nucleases, base editors, transposases and prime editors. Nat Biotechnol 2020;38:824-44.
