ArticleCommunications biology2025
MRG15 alternative splicing regulates CDK1 transcriptional activity in mouse cell senescence and myocardial regeneration.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- MORF4L1 regulation and its role in chromatin remodeling, DNA damage, cellular senescence, and cardiometabolic disease.Vascular pharmacology · 2026Review
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- Elucidating Gene Functions in Congenital Heart Disease.Current treatment options in cardiovascular medicine · 2026Review
- Alternative Splicing: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- Transcript diversity in aging: cryptic transcription and splicing.Medical review (2021) · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
MRG15, a chromatin remodeling protein, plays a pivotal role in cellular senescence and proliferation. However, the precise roles and mechanisms of MRG15 in aging regulation remain unclear. Our research elucidates the distinct functions of MRG15's splice variants in aging. We find that MRG15L, contrary to the previously assumed MRG15S, accumulates with advancing age. Using histone peptide binding assays and protein interaction analysis, we demonstrate that MRG15L exhibits reduced affinity for histone H4 acetylation sites, thereby weakening CDK1 regulation, leading to G2/M phase arrest and promoting cellular senescence. During postnatal cardiac development, MRG15L expression increases and is linked to reduced regenerative capacity. Moreover, targeted knockout of MRG15L in mice enhances cardiac repair and regeneration following myocardial ischemia-reperfusion injury. These findings highlight MRG15L as a promising therapeutic target for age-related diseases, revealing its critical role in modulating aging pathways through alternative splicing.
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Registered trials
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