ArticleMolecular therapy. Nucleic acids2021
Exosomal LINC00174 derived from vascular endothelial cells attenuates myocardial I/R injury via p53-mediated autophagy and apoptosis.
Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
- Vascular endothelial cell-derived small extracellular vesicles: A protective role against cardiomyocyte apoptosis in ischemia-reperfusion injury through miR410-3p-modulatedThe Journal of international medical research · 2026Article
- MSC-Derived Exosomes in Preserving Autophagy through Key Signaling Pathways: A Preventive Strategy against Cardiovascular Aging.Cell biochemistry and biophysics · 2026Review
- Exosomes Enhance Diagnosis and Therapy of Ischemic Heart Disease: Insights and Advances.Journal of cardiovascular translational research · 2026Review
- The multifaceted roles of non-coding RNAs in cell-cell communication in cardiovascular health and disease.Cell & bioscience · 2025Review
- The PIWI-interacting RNA CRAPIR alleviates myocardial ischemia‒reperfusion injury by reducing p53-mediated apoptosis via binding to SRSF1.Acta pharmacologica Sinica · 2025Article
- Mitochondrial dysfunction in AMI: mechanisms and therapeutic perspectives.Journal of translational medicine · 2025Review
- The Role of P53 in Myocardial Ischemia-Reperfusion Injury.Cardiovascular drugs and therapy · 2025Review
- The role of exosomal lncRNAs in cardiovascular disease: Emerging insights based on molecular mechanisms and therapeutic target level.Non-coding RNA research · 2025Review
- Comprehensive evaluation of non-coding RNA-mediated autophagy regulation in myocardial ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- Splicing factor SRSF1 attenuates cardiomyocytes apoptosis via regulating alternative splicing of Bcl2L12.Cell & bioscience · 2024Article
- Gastrodin prevents myocardial injury in sleep-deprived mice by suppressing ferroptosis through SIRT6.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Queen bee acid pretreatment attenuates myocardial ischemia/reperfusion injury by enhancing autophagic flux.Heliyon · 2024Article
- Extracellular vesicles originating from the mechanical microenvironment in the pathogenesis and applications for cardiovascular diseases.Regenerative therapy · 2024Review
- Crosstalk among Reactive Oxygen Species, Autophagy and Metabolism in Myocardial Ischemia and Reperfusion Stages.Aging and disease · 2024Review
- Vascular Endothelial Cell-Derived Exosomal Sphingosylphosphorylcholine Attenuates Myocardial Ischemia-Reperfusion Injury through NR4A2-Mediated Mitophagy.International journal of molecular sciences · 2024Article
- Exosomes-Mediated Signaling Pathway: A New Direction for Treatment of Organ Ischemia-Reperfusion Injury.Biomedicines · 2024Review
- Review
- Uncovering periodontitis-associated markers through the aggregation of transcriptomics information from diverse sources.Frontiers in genetics · 2024Article
- Cardiac cells and mesenchymal stem cells derived extracellular vesicles: a potential therapeutic strategy for myocardial infarction.Frontiers in cardiovascular medicine · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we aim to investigate the regulation of specific long non-coding RNAs (lncRNAs) on the progression of ischemia/reperfusion (I/R) injury. We identified and characterized the exosomes derived from mouse primary aortic endothelial cells. Subsequently, we found that these exosomes expressed typical exosomal markers and high levels of LINC00174, which significantly ameliorated I/R-induced myocardial damage and suppressed the apoptosis, vacuolation, and autophagy of myocardial cells. Mechanistic approaches revealed that LINC00174 directly interacted with SRSF1 to suppress the expression of p53, thus restraining the transcription of myocardin and repressing the activation of the Akt/AMPK pathway that was crucial for autophagy initiation in I/R-induced myocardial damage. Moreover, this molecular mechanism was verified by
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