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ArticleOnline now102856Open access Affiliations & Notes 1Division of Cardiovascular Medicine, Department of Internal Medicine, School of Medicine, University of California, Davis, Sacramento, CA 95817, USA 2Department of Radiation Oncology, University of California, Davis, Sacramento, CA 95817, USA 3Department of Entomology and Nematology, and Comprehensive Cancer Center, University of California, Davis, Davis, CA 95616, USA 4Department of Neurobiology, Physiology, and Behavior, University of...
Correction to: Nature Communications https://doi.org/10.1038/s41467-024-47847-8, published online 25 April 2024 The peer review file was originally published with confidential data intended solely for the Reviewers and Editors; this material has now been redacted and the peer review file has now been replaced with the correct redacted version.
Abstract Cardiac dysfunction is a hallmark of aging in humans and mice. Here we report that a two-week treatment to restore youthful Bridging Integrator 1 (BIN1) levels in the hearts of 24-month-old mice rejuvenates cardiac function and substantially reverses the aging phenotype. Our data indicate that age-associated overexpression of BIN1 occurs alongside dysregulated endosomal recycling and disrupted trafficking of cardiac CaV1.2 and type 2 ryanodine receptors.
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