ArticleJournal of the Chinese Medical Association : JCMA2024
Exosomal MALAT1 from macrophages treated with high levels of glucose upregulates LC3B expression via miR-204-5p downregulation.
Article in Journal of the Chinese Medical Association : JCMA, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 5 citations in OpenAlex.
- Epigallocatechin-3-gallate Modulates Hyperglycemia-Triggered Macrophage Autophagy Through miR-204-5p Suppression: Implication for Acute Cardiometabloic Injury.Journal of acute medicine · 2026Article
- Article
- Suppressive effect of chrysin on macrophage LC3B autophagy through miR-204-5p in diabetic atherosclerosis.Scientific reports · 2026Article
- Knockdown of Long Non-coding RNA-MALAT1 Ameliorates Diabetic Lower Limb Atherosclerotic Disease Through MiR-17-5p-Mediated Endothelial Cell Pyroptosis.Biochemical genetics · 2026Article
- Harnessing exosomal long non-coding RNAs as a new frontier for molecular diagnostics and therapeutics in diabetes mellitus.Cell communication and signaling : CCS · 2026Review
- Exosomal MicroRNA-1 Regulate Cx43 Expression via Tbx18 in Culture Atrial Fibroblasts under Rapid Electrical Stimulation.Acta Cardiologica Sinica · 2026Article
- Exo-hydrogel therapy: a revolutionary approach to managing diabetic complications.Journal of nanobiotechnology · 2025Review
- Macrophage-Derived Exosomal MALAT1 Regulates Autophagy through miR-204-5p/ATG7 Axis in H9C2 Cardiomyocytes and Diabetic Rat Heart.Acta Cardiologica Sinica · 2025Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundMetastasis-associated lung adenocarcinoma transcript 1 ( MALAT1 ) plays a critical role in the pathophysiology of diabetes-related complications. However, whether macrophage-derived MALAT1 affects autophagic activity under hyperglycemic conditions is unclear. Therefore, we investigated the molecular regulatory mechanisms of macrophage-derived MALAT1 and autophagy under hyperglycemic conditions.
methodsHyperglycemia was induced by culturing macrophages in 25 mM glucose for 1 hour. Exosomes were extracted from the culture media. A rat model of carotid artery balloon injury was established to assess the effect of MALAT1 on vascular injury. Reverse transcription, real-time quantitative polymerase chain reaction, western blotting, immunohistochemical staining, and luciferase activity assays were performed.
resultsStimulation with high levels of glucose significantly enhanced MALAT1 expression in macrophage-derived exosomes. MALAT1 inhibited miR-204-5p expression in macrophage-derived exosomes under hyperglycemic conditions. siRNA-induced silencing of MALAT1 significantly reversed macrophage-derived exosome-induced miR-204-5p expression. Hyperglycemic treatment caused a significant, exosome-induced increase in the expression of the autophagy marker LC3B in macrophages. Silencing MALAT1 and overexpression of miR-204-5p significantly decreased LC3B expression induced by macrophage-derived exosomes. Overexpression of miR-204-5p significantly reduced LC3B luciferase activity induced by macrophage-derived exosomes. Balloon injury to the carotid artery in rats significantly enhanced MALAT1 and LC3B expression, and significantly reduced miR-204-5p expression in carotid artery tissue. Silencing MALAT1 significantly reversed miR-204-5p expression in carotid artery tissue after balloon injury. MALAT1 silencing or miR-204-5p overexpression significantly reduced LC3B expression after balloon injury.
conclusionThis study demonstrated that hyperglycemia upregulates MALAT1 . MALAT1 suppresses miR-204-5p expression and counteracts the inhibitory effect of miR-204-5p on LC3B expression in macrophages to promote vascular disease.
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