ArticleBioactive materials2025
Delivering LINE1 antisense oligonucleotides via endothelial targeting extracellular vesicles to ameliorate myocardial infarction-induced cardiac senescence.
Article in Bioactive materials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The therapeutic potential of transposable element activity modulation.EMBO molecular medicine · 2026Review
- Macrophage PARP7 Alleviates Septic Cardiomyopathy by Interacting With TBK1 and Suppressing TBK1-Driven Inflammatory Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Alix-mediated selective packaging of β-catenin into extracellular vesicles enhances their proangiogenic function.The Journal of biological chemistry · 2026Article
- Mitochondrial homeostasis and aging: the mtDNA-cGAS-STING axis.Frontiers in immunology · 2026Review
- Activation of the cGAS-STING Pathway by NETs Promotes Inflammatory Injury in Myocardial Ischemia-Reperfusion.Journal of inflammation research · 2026Article
- Therapeutic advances in spinal muscular atrophy: a review of clinical, safety, and economic considerations.Frontiers in pharmacology · 2026Review
- Cellular senescence and polycystic ovary syndrome: mechanisms and therapeutic strategies from a new perspective.Annals of medicine · 2025Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transposable elements (TEs) constitute a significant portion of the nuclear genome, but their influence on and ability to manage their activity during tissue regeneration remain largely unknown. Here, we revealed that LINE1, the most abundant TE, responds to cardiomyocyte injury and is overexpressed in a myocardial infarction (MI) model. We developed selectin binding peptide (SBP)-engineered extracellular vesicles (EVs) with targeted functions, which are loaded with LINE1 antisense oligonucleotide (ASO). The engineered EVs display targeted accumulation in injured hearts and protect against myocardial senescence by inhibiting the cGAS-STING-TBK1-IRF3 pathway and suppressing the expression of senescence-associated secretory phenotype (SASP) factors. Our data revealed that LINE1 retrotransposon activation is triggered by cardiomyocyte injury in the MI model. We also propose a strategy to reduce cardiomyocyte senescence post-myocardial infarction by modulating LINE1 activity.
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Registered trials
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