ArticleBiochemical and biophysical research communications2025
Novel therapeutic cav1.3-C-terminus normalizes L-type calcium current and ejection fraction in ischemia-induced murine heart failure.
Article in Biochemical and biophysical research communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Impact of CaInternational journal of molecular sciences · 2026Review
- C-Terminus of CaCells · 2026Article
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6 authors.
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Abstract
introductionHeart failure (HF) affects approximately 6.7 million Americans and rising. Despite multi-modality therapy, patient outcomes remain suboptimal. It has been recently shown that Cav1.3 L-type calcium channels are re-expressed in ischemic failing human ventricles, and the Cav1.3-C-terminus is cleaved and acts as a transcription factor. Here, we leveraged the Cav1.3-C-terminus's auto-enhancer properties as a novel therapy to restore ejection fraction (EF) in HF.
methodsHF was established in wild-type (WT) and Cav1.3-heterozygous-knockout (Cav1.3
resultsAt day 15 post-LAD-ligation, WT-HF mice displayed fibrosis, impaired wall motion, increased left ventricular diameter in diastole and systole, and decreased left ventricular EF and fractional shortening vs. WT-Sham. Cav1.3 mRNA/protein levels increased in WT-HF mice vs. WT-Sham. At day 30 post-AAV9-Cav1.3-C-terminus-treatment, WT-Sham and Cav1.3
conclusionsAAV9-Cav1.3-C-terminus-treatment of mice with HF resulted in resistance to inducible arrhythmia and normalization of left ventricular EF, likely via a transcriptional upregulation of Cav1.3 and the resulting optimal increase in L-type calcium current. Therefore, AAV9-Cav1.3-C-terminus may be leveraged as a novel therapeutic approach to improve cardiac function.
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