Mol Ther Nucleic AcidsJClub
lncRNA Lockd promotes cardiomyocyte proliferation via Eno1/beta-catenin/Myc axis.
Molecular therapy. Nucleic acids · · Journal Article · Open access
Prakash, Kundu + more
Abstract ↗AI summary
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Lockd overexpression in non-regenerative neonatal mouse hearts attenuates isoproterenol-induced pathological hypertrophy and restores cardiomyocyte proliferation via the ENO1/β-catenin/Myc axis.
- Why it matters: Neonatal hearts can regenerate only during a limited window, but how they resist pathological hypertrophic stress outside that period is unclear.
- What they did: Neonatal hearts were challenged with isoproterenol across regenerative versus non-regenerative phases, and transcriptomics highlighted Lockd as the top upregulated lncRNA in an E2F1-dependent manner; cardiomyocyte-specific AAV9 Lockd overexpression tested function.
- The result: Lockd directly interacts with and stabilizes ENO1, increasing β-catenin stability and nuclear accumulation and inducing Myc, while ENO1 knockdown impaired β-catenin signaling, Myc expression, and cardiomyocyte proliferation.
The findingWhy it mattersWhat they didThe result
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