ArticleInternational journal of molecular sciences2022
Exosomal MALAT1 Derived from High Glucose-Treated Macrophages Up-Regulates Resistin Expression via miR-150-5p Downregulation.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- 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
- Article
- The multifaceted roles of non-coding RNAs in cell-cell communication in cardiovascular health and disease.Cell & bioscience · 2025Review
- Exosomal transfer of miR-375-3p from pancreatic β cells to hepatocytes impairs hepatic glycogenesisWorld journal of diabetes · 2025Article
- Extracellular vesicles in cancer immunotherapy: Therapeutic, challenges and clinical progress.Asian journal of pharmaceutical sciences · 2025Review
- Macrophage-Derived Exosomal MALAT1 Regulates Autophagy through miR-204-5p/ATG7 Axis in H9C2 Cardiomyocytes and Diabetic Rat Heart.Acta Cardiologica Sinica · 2025Article
- Macrophage-derived lncRNAs in cancer: regulators of tumor progression and therapeutic targets.Medical oncology (Northwood, London, England) · 2025Review
- Regulation of lipid metabolism in grass carp primary hepatocytes by exosomes derived from fatty hepatocytes though GRP78.Fish physiology and biochemistry · 2024Article
- Article
- Exosomes and Macrophages: Bidirectional Mutual Regulation in the Treatment of Diabetic Complications.Cellular and molecular bioengineering · 2024Review
- Review
- Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- Extracellular Vesicles and Immunity: At the Crossroads of Cell Communication.International journal of molecular sciences · 2024Review
- The Immunomodulatory effect of exosomes in diabetes: a novel and attractive therapeutic tool in diabetes therapy.Frontiers in immunology · 2024Review
- Targeting lncRNA MALAT1: A Promising Approach to Overcome Metabolic Syndrome.International journal of endocrinology · 2024Review
- Macrophage-derived extracellular vesicles as new players in chronic non-communicable diseases.Frontiers in immunology · 2024Review
- Extracellular vesicles: mechanisms and prospects in type 2 diabetes and its complications.Frontiers in endocrinology · 2024Review
- Roles of long noncoding RNAs and small extracellular vesicle-long noncoding RNAs in type 2 diabetes.Traffic (Copenhagen, Denmark) · 2022Review
- Exosomal microRNAs in diabetic heart disease.Cardiovascular diabetology · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a crucial role in the pathophysiological process associated with diabetes-related complications. The effect of high glucose levels on macrophage-derived exosomal MALAT1 is unknown. Therefore, we investigated the molecular regulatory mechanisms controlling exosomal MALAT1 in macrophages under high glucose treatment and the therapeutic target of macrophage-derived exosomal MALAT1 using a balloon injury model of vascular disease in diabetic rats. High glucose (25 mM) significantly increased MALAT1 expression in macrophage-derived exosomes. MALAT1 suppressed miR-150-5p expression in macrophage-derived exosomes under high-glucose conditions. Silencing MALAT1 using MALAT1 siRNA significantly reversed miR-150-5p expression induced by macrophage-derived exosomes. Macrophage-derived exosomes under high-glucose treatment significantly increased resistin expression in macrophages. Silencing MALAT1 and overexpression of miR-150-5p significantly decreased resistin expression induced by macrophage-derived exosomes. Overexpression of miR-150-5p significantly decreased resistin luciferase activity induced by macrophage-derived exosomes. Macrophage-derived exosome significantly decreased glucose uptake in macrophages and silencing MALAT1, resistin or overexpression of miR-150-5p significantly reversed glucose uptake. Balloon injury to the carotid artery significantly increased MALAT1 and resistin expression and significantly decreased miR-150-5p expression in arterial tissue. Silencing MALAT1 significantly reversed miR-150-5p expression in arterial tissue after balloon injury. Silencing MALAT1 or overexpression of miR-150-5p significantly reduced resistin expression after balloon injury. In conclusion, high glucose up-regulates MALAT1 to suppress miR-150-5p expression and counteracts the inhibitory effect of miR-150-5p on resistin expression in macrophages to promote vascular disease. Macrophage-derived exosomes containing MALAT1 may serve as a novel cell-free approach for the treatment of vascular disease in diabetes mellitus.
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