ArticleInternational journal of nanomedicine2020
Exosomal lncRNA AK139128 Derived from Hypoxic Cardiomyocytes Promotes Apoptosis and Inhibits Cell Proliferation in Cardiac Fibroblasts.
Article in International journal of nanomedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- Engineering extracellular vesicles for targeted therapeutic delivery in the heart.Bioscience reports · 2026Review
- Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Extracellular vesicles in heart failure: bridging pathogenic insights, diagnostic utility, and therapeutic applications.Frontiers in pharmacology · 2026Review
- Hypoxic Small Extracellular Vesicle Preconditioning of AC16 Cardiomyocytes Increase Caspase-3 and Caspase-8 Activity During Hypoxia.International journal of molecular sciences · 2025Article
- Extracellular Vesicles in Cardiovascular Diseases: Signaling, Biomarker, and Therapy.Journal of cardiovascular translational research · 2025Review
- Circulating Extracellular Vesicles from Heart Failure Patients Inhibit Human Cardiomyocyte Activities.Journal of cardiovascular translational research · 2025Article
- The multifaceted roles of non-coding RNAs in cell-cell communication in cardiovascular health and disease.Cell & bioscience · 2025Review
- The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review.Non-coding RNA research · 2025Review
- The biology of exosomes and exosomal non-coding RNAs in cardiovascular diseases.Frontiers in pharmacology · 2025Review
- Extracellular vesicles: molecular messengers and new therapeutic targets in acute myocardial infarction.Frontiers in immunology · 2025Review
- Harnessing exosomes in theranostic applications: advancements and insights in gastrointestinal cancer research.Discover oncology · 2024Review
- Review
- LIPCAR levels in plasma-derived extracellular vesicles is associated with left ventricle remodeling post-myocardial infarction.Journal of translational medicine · 2024Article
- Exosomes Induce Crosstalk Between Multiple Types of Cells and Cardiac Fibroblasts: Therapeutic Potential for Remodeling After Myocardial Infarction.International journal of nanomedicine · 2024Review
- Research progress of exosomes from different sources in myocardial ischemia.Frontiers in cardiovascular medicine · 2024Review
- Identification and functional analysis of circulating small extracellular vesicle lncRNA signatures in children with fulminant myocarditis.Journal of cellular and molecular medicine · 2024Article
- Cardiac cells and mesenchymal stem cells derived extracellular vesicles: a potential therapeutic strategy for myocardial infarction.Frontiers in cardiovascular medicine · 2024Review
- Advances in Intercellular Communication Mediated by Exosomal ncRNAs in Cardiovascular Disease.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionMyocardial infarction (MI) is the leading cause of congestive heart failure and mortality. Hypoxia is an important trigger in the cardiac remodeling of the myocardium in the development and progression of cardiac diseases.
objectiveThus, we aimed to investigate the effect of hypoxia-induced exosomes on cardiac fibroblasts (CFs) and its related mechanisms. MATERIALS AND
methodsIn this study, we successfully isolated and identified the exosomes from hypoxic cardiomyocytes (CMs). Exosomes derived from hypoxic CMs promoted apoptosis and inhibited proliferation, migration, and invasion in CFs. RNA-Seq assay suggested that long noncoding RNA AK139128 (lncRNA AK139128) was found to overexpress in both hypoxic CMs and CMs-secreting exosomes. After coculturing with CFs, hypoxic exosomes increased the expression of AK139128 in recipient CFs. Moreover, exosomal AK139128 derived from hypoxic CMs stimulated CFs apoptosis and inhibited proliferation, migration, and invasion. Furthermore, the effect of exosomal AK139128 derived from hypoxic CMs could also exacerbate MI in the rat model.
conclusionTaken together, hypoxia upregulated the level of AK139128 in CMs and exosomes and exosomal AK139128 derived from hypoxic CMs modulated cellular activities of CFs in vitro and in vivo. This study provides a new understanding of the mechanism underlying hypoxia-related cardiac diseases and insight into developing new therapeutic strategies.
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Registered trials
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