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by inhibitor 1 of protein phosphatase 1 (I1PP1), is vital for maintaining cardiovascular homeostasis. However, the role and mechanism of I1PP1 against hypoxia-reoxygenation (H\/R) injury in cardiomyocytes remain a question. In our study, after I1PP1 overexpression by adenovirus infection in the neonatal cardiomyocytes followed by hypoxia for 4\u2009h and reoxygenation for 12\u2009h, the CaMKII<jats:italic>\u03b4<\/jats:italic> alternative splicing subtype, ATP content, and lactate dehydrogenase (LDH) release were determined. CaMKII activity was evaluated by phosphoprotein phosphorylation at Thr17 (p-PLB Thr17), CaMKII phosphorylation (p-CaMKII), and CaMKII oxidation (ox-CaMKII). Reactive oxygen species (ROS), mitochondrial membrane potential, dynamin-related protein 1 (DRP1), and optic atrophy 1 (OPA1) expressions were assessed. Our study verified that I1PP1 overexpression attenuated the CaMKII<jats:italic>\u03b4<\/jats:italic> alternative splicing disorder; suppressed PLB phosphorylation at Thr17, p-CaMKII, and ox-CaMKII; decreased cell LDH release; increased ATP content; attenuated ROS production; increased mitochondrial membrane potential; and decreased DRP1 expression but increased OPA1 expression in the cardiomyocytes after H\/R. Contrarily, CaMKII<jats:italic>\u03b4<\/jats:italic> alternative splicing disorder, LDH release, ATP reduction, and ROS accumulation were aggravated after H\/R injury with the I1PP1 knockdown. Collectively, I1PP1 overexpression corrected disorders of CaMKII<jats:italic>\u03b4<\/jats:italic> alternative splicing, inhibited CaMKII phosphorylation, repressed CaMKII oxidation, suppressed ROS production, and attenuated cardiomyocyte H\/R injury.<\/jats:p>","DOI":"10.1155\/2019\/2193019","type":"journal-article","created":{"date-parts":[[2019,12,7]],"date-time":"2019-12-07T18:30:18Z","timestamp":1575743418000},"page":"1-19","source":"Crossref","is-referenced-by-count":15,"title":["Inhibitor 1 of Protein Phosphatase 1 Regulates Ca<sup>2+<\/sup>\/Calmodulin-Dependent Protein Kinase II to Alleviate Oxidative Stress in Hypoxia-Reoxygenation Injury of Cardiomyocytes"],"prefix":"10.1155","volume":"2019","author":[{"given":"Huiqin","family":"Luo","sequence":"first","affiliation":[{"name":"Department of Pharmacology, School of Pharmacy, Nantong University, Key Laboratory of Inflammation and Molecular Drug Target of Jiangsu Province, Nantong, Jiangsu, 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