ArticleInternational journal of nanomedicine2025
Lymph Node Exosomes Delivery Attenuates Myocardial Ischemia-Reperfusion Injury via Regulating PTEN-PI3K/Akt Pathway Mediated Myocardiocyte Apoptosis.
Article in International journal of nanomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- PIP3 antagonist as a molecular regulator in MSC-derived cardiomyocytes: Potential in vitro therapeutic implications for conotruncal heart defects.Journal, genetic engineering & biotechnology · 2026Article
- 3D-bioprinted mesenchymal stem cell-derived exosomes reprogram macrophages via PI3K/AKT to accelerate nerve regeneration.Journal of translational medicine · 2026Article
- Exosomes in inflammatory tissue injury: key pathogenic factors and promising therapeutic agents.Frontiers in immunology · 2026Review
- Targeting the heart-immune axis after myocardial infarction: from inflammation to immunomodulation.Frontiers in cardiovascular medicine · 2026Review
- Cardiac Development, Cellular Composition and Function: From Regulatory Mechanisms to Applications.Cells · 2025Review
- Advanced Nanomaterial Platforms for Targeted Therapy of Myocardial Ischemia-Reperfusion Injury.Research (Washington, D.C.) · 2025Review
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Authors and funding
7 authors.
Funding
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Abstract
Background: Ischemia/reperfusion (I/R) injury following acute myocardial infarction (AMI) induces myocardial apoptosis. Exosomes from KLF2-overexpressing endothelial cells (KLF2-EXO) dampened the effects of I/R injury. The intra-lymph node drainage pathway provides an alternative method to study the therapeutic effects of exosomes. In this study, we explored the role of intra-lymph node injection of KLF2-EXO in myocardial I/R injury. Method and Result: Exosomes were isolated from KLF2-overexpressing mouse coronary endothelial cell supernatant via gradient centrifugation. The mice were subjected to ischemia and reperfusion, and an appropriate dosage of KLF2-EXO was administrated via intra-inguinal lymph node injection. KLF2-EXO attenuated I/R injury and alleviated myocardiocyte apoptosis in heart tissue, and immunofluorescence staining indicated KLF2-EXO could be transferred into the heart. MiRNA-sequencing of KLF2-EXO implicated that miRNA-486-5p (miR-486-5p) was a potent candidate mediator that inhibited myocardiocyte apoptosis, and the miR-486-5p antagomir reversed the effect. Further bioinformatics analysis and confirmation experiments revealed that PTEN functions as a downstream target and that the PTEN- PI3K/Akt pathway participates in the regulation of cardiomyocyte apoptosis. Conclusion: Our data demonstrated that intra-lymph node injection of KLF2-EXO attenuated myocardial I/R injury in mice by delivering miR-486-5p to target PTEN- PI3K/Akt pathway, which restrained myocardiocyte apoptosis. KLF2-EXO may serve as an alternative therapy for myocardial I/R injury.
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