ArticleScientific reports2024
Loss of connectin novex-3 leads to heart dysfunction associated with impaired cardiomyocyte proliferation and abnormal nuclear mechanics.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Nx3 Is a Z-Disk Structural and Signaling Hub That Is Reduced in Heart Failure.Circulation research · 2026Article
- Big Job for the Small Titin: Don't Underestimate the "Little" Guy.Circulation research · 2026Article
- Phosphorescence lifetime microscopy and contrast-enhanced ultrasound imaging revealed strong left-to-right intraventricular shunt in anesthetized Xenopus laevis.The journal of physiological sciences : JPS · 2026Article
- CCDC141 is a Connectin/Titin and Nesprin-1 binding protein that adapts cardiomyocytes to mechanical stress.Communications biology · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
Connectin (also known as titin) is a giant striated muscle protein that functions as a molecular spring by providing elasticity to the sarcomere. Novex-3 is a short splice variant of connectin whose physiological function remains unknown. We have recently demonstrated using in vitro analyses that in addition to sarcomere expression, novex-3 was also expressed in cardiomyocyte nuclei exclusively during fetal life, where it provides elasticity/compliance to cardiomyocyte nuclei and promotes cardiomyocyte proliferation in the fetus, suggesting a non-sarcomeric function. Here, we analyzed novex-3 knockout mice to assess the involvement of this function in cardiac pathophysiology in vivo. Deficiency of novex-3 compromised fetal cardiomyocyte proliferation and induced the enlargement of individual cardiomyocytes in neonates. In adults, novex-3 deficiency resulted in chamber dilation and systolic dysfunction, associated with Ca
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