ArticleCirculation2023
Elimination of CaMKIIδ Autophosphorylation by CRISPR-Cas9 Base Editing Improves Survival and Cardiac Function in Heart Failure in Mice.
Article in Circulation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Novel Quality Metrics for Assessing the Reproducibility and Translational Relevance of Mouse Transverse Aortic Constriction Experiments: A Systematic Review.Journal of the American Heart Association · 2026Pooled it
- Next-Generation Bone Marrow Cell Therapies for Cardiac Repair: Integrating Gene Therapy and Bioengineering to Enhance Therapeutic Potency.Journal of cardiovascular translational research · 2026Review
- Base editing for precision therapeutics.Cell genomics · 2026Review
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- Precision modification of heart failure signaling by CRISPR-Cas9 base editing.Journal of molecular and cellular cardiology · 2026Review
- Yiqi Huoxue formula relieves heart failure with reduced ejection fraction in calcium/calmodulin-dependent protein kinase Ⅱ delta B isoform and calcium/calmodulin-dependent protein kinase Ⅱ delta C isoform transgenic mice by inhibiting myocardial remodeling and enhancing calcium homeostasis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Structural and Functional Regulation of RyR2 in Cardiac Calcium Handling and Arrhythmogenesis.Biomedicines · 2026Review
- Myocardial Recovery With Mechanical Circulatory Support Is Linked to Alternative Splicing and Subcellular Localization of CAMK2D.Circulation · 2026Article
- Danhong Injection targets CaMKII through Dihydrotanshinone I to alleviate cardiomyocyte death and inflammation in viral myocarditis.Science China. Life sciences · 2026Article
- Research on the effect of augmented reality based sensory interaction device in rehabilitation training of patients with chronic heart failure.BMC cardiovascular disorders · 2026Article
- Gene Editing Applications as Future Cardiovascular Therapies.Annual review of genetics · 2025Review
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- Harnessing extracellular vesicles to deliver genetic medicine for cardiac repair.Nanomedicine (London, England) · 2025Article
- Molecular Mechanisms of L-Type Calcium Channel Dysregulation in Heart Failure.International journal of molecular sciences · 2025Review
- Cytoplasmic CaMKIIδ-B prevents myocardial recovery in heart failure.bioRxiv : the preprint server for biology · 2025Article
- Increased MyocardialInternational journal of molecular sciences · 2025Article
- MyocardialAntioxidants (Basel, Switzerland) · 2025Article
- Bioinformatics-driven insights: rapamycin-mediated CaMK2D inhibition alleviates intestinal ischemia-reperfusion injury.Frontiers in immunology · 2025Article
- Gene editing therapy as a therapeutic approach for cardiovascular diseases in animal models: A scoping review.PloS one · 2025Article
- Empagliflozin prevents heart failure through inhibition of the NHE1-NO pathway, independent of SGLT2.Basic research in cardiology · 2024Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundCardiovascular diseases are the main cause of worldwide morbidity and mortality, highlighting the need for new therapeutic strategies. Autophosphorylation and subsequent overactivation of the cardiac stress-responsive enzyme CaMKIIδ (Ca
methodsTo develop a comprehensive therapy for heart failure, we used CRISPR-Cas9 adenine base editing to ablate the autophosphorylation site of CaMKIIδ. We generated mice harboring a phospho-resistant CaMKIIδ mutation in the germline and subjected these mice to severe transverse aortic constriction, a model for heart failure. Cardiac function, transcriptional changes, apoptosis, and fibrosis were assessed by echocardiography, RNA sequencing, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and standard histology, respectively. Specificity toward
resultsWithin 2 weeks after severe transverse aortic constriction surgery, 65% of all wild-type mice died, and the surviving mice showed dramatically impaired cardiac function. In contrast to wild-type mice, CaMKIIδ phospho-resistant gene-edited mice showed a mortality rate of only 11% and exhibited substantially improved cardiac function after severe transverse aortic constriction. Moreover, CaMKIIδ phospho-resistant mice were protected from heart failure-related aberrant changes in cardiac gene expression, myocardial apoptosis, and subsequent fibrosis, which were observed in wild-type mice after severe transverse aortic constriction. On the basis of identical mouse and human genome sequences encoding the autophosphorylation site of
conclusionsAblation of CaMKIIδ autophosphorylation by adenine base editing may offer a potential broad-based therapeutic concept for human cardiac disease.
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