ArticleCell and tissue research2022
Plasma-derived extracellular vesicles transfer microRNA-130a-3p to alleviate myocardial ischemia/reperfusion injury by targeting ATG16L1.
Article in Cell and tissue research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
10 citing papers in PubMed, 10 citations in OpenAlex.
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- Integrated Assessment of Metabolic, Oxidative, and Molecular Adaptations from Pregnancy to Early Lactation in Shami Goats (Veterinary sciences · 2026Article
- Plasma-Derived Extracellular Vesicles Inhibit Lipopolysaccharide-Induced Apoptosis and Oxidative Stress in Human AC16 Cardiomyocytes.Current issues in molecular biology · 2026Article
- Extracellular vesicles for delivering therapeutic agents in ischemia/reperfusion injury.Asian journal of pharmaceutical sciences · 2024Article
- Review
- Exosomes as Vehicles for Noncoding RNA in Modulating Inflammation: A Promising Regulatory Approach for Ischemic Stroke and Myocardial Infarction.Journal of inflammation research · 2024Review
- Article
- Mechanisms and therapeutic strategies of extracellular vesicles in cardiovascular diseases.MedComm · 2023Review
- Therapeutic Potential of EVs: Targeting Cardiovascular Diseases.Biomedicines · 2023Review
- A bibliometric analysis of myocardial ischemia/reperfusion injury from 2000 to 2023.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Extracellular vesicles (EVs) are implicated in myocardial ischemia/reperfusion (I/R) injury as modulators by shuttling diverse cargoes, including microRNAs (miRNAs). The current study was initiated to unravel the potential involvement of plasma-derived EVs carrying miR-130a-3p on myocardial I/R injury. Rats were induced with moderate endoplasmic reticulum stress, followed by isolation of plasma-derived EVs. Then, an I/R rat model and hypoxia/reoxygenation (H/R) cardiomyoblast model were established to simulate a myocardial I/R injury environment where miR-130a-3p was found to be abundantly expressed. miR-130a-3p was confirmed to target and negatively regulate autophagy-related 16-like 1 (ATG16L1) in cardiomyoblasts. Based on a co-culture system, miR-130a-3p delivered by EVs derived from plasma protected H/R-exposed cardiomyoblasts against H/R-induced excessive cardiomyoblast autophagy, inflammation, and damage, improving cardiac dysfunction as well as myocardial I/R-induced cardiac dysfunction and tissue injury. The mechanism underlying the functional role of EVs-loaded miR-130a-3p was found to be dependent on its targeting relation with ATG16L1. The protective action of EV-carried miR-130a-3p was further re-produced in a rat model serving as in vivo validation as evidenced by improved cardiac function, tissue injury, myocardial fibrosis, and myocardial infarction. Collectively, miR-130a-3p shuttled by plasma-derived EVs was demonstrated to alleviate excessive cardiomyoblast autophagy and improve myocardial I/R injury.
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Registered trials
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