ArticleActa Cardiologica Sinica2025
Macrophage-Derived Exosomal MALAT1 Regulates Autophagy through miR-204-5p/ATG7 Axis in H9C2 Cardiomyocytes and Diabetic Rat Heart.
Article in Acta Cardiologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Elevated Metastasis-Associated lung adenocarcinoma transcript 1 (MALAT1) expression predicts coronary artery disease severity as a potential biomarker for risk stratification: a cross-sectional study.Annals of medicine · 2026Article
- Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Review
- Advances in the application of nanoparticles for the diagnosis and treatment of diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- Article
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4 authors.
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Abstract
Background: Autophagy activity is tightly associated with cardiovascular disease development and progression. The effect of exosomal metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) derived from macrophages treated with high levels of glucose on autophagy in cardiomyocytes and diabetic hearts is not known. We investigated the effect of autophagy and its regulatory mechanisms on H9C2 cardiomyocytes and diabetic hearts by macrophage-derived exosomal MALAT1. Methods: Mouse macrophages and rat H9C2 cardiomyocytes were cultured, and exosomes were extracted from the culture media. A diabetic model was established through the injection of streptozotocin into adult male Wistar rats. Reverse transcription real-time quantitative polymerase chain reaction, Western blotting, immunohistochemical staining, autophagosome and/or autolysosome fluorescent cell staining, and luciferase activity assays were performed. Results: High glucose significantly enhanced exosomal MALAT1 expression in cultured H9C2 cells and macrophages. Macrophage-derived exosomes significantly increased autophagy-related 7 (ATG7) and decreased miR-204-5p expressions. Silencing MALAT1 by MALAT1 small interference RNA and the overexpression of wild-type miR-204-5p significantly decreased the ATG7 expression induced by macrophage-derived exosomes. MiR-204-5p significantly decreased MALAT1 and ATG7 luciferase activity in cultured H9C2 cells treated with macrophage-derived exosomes. Streptozotocin-induced diabetes mellitus and macrophage-derived exosomes significantly enhanced MALAT1 expression to inhibit miR204-5p expression in the rat hearts. Macrophage-derived exosomes significantly enhanced ATG7 expression in the streptozotocin-induced diabetic hearts. Conclusions: In conclusion, we discovered that exosomal MALAT1 derived from macrophages after high glucose treatment could sequester miR-204-5p, leading to the upregulation of ATG7 expression, and this was linked to the regulation of autophagy in H9C2 cardiomyocytes and streptozotocin-induced diabetic hearts.
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