ArticleClinical and experimental nephrology2024
METTL14 derived from exosomes of M1 macrophages promotes high glucose-induced apoptosis, inflammation and oxidative stress in glomerular endothelial cells by mediating PAQR3 m6A modification.
Article in Clinical and experimental nephrology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exosomes in diabetic kidney disease: pathogenesis, biomarker discovery, and emerging therapeutics-a comprehensive systematic review.Renal failure · 2026Pooled it
- M1 macrophage-derived exosomes aggravate diabetic nephropathy by regulating the WTAP/S1PR2 axis.Journal of diabetes investigation · 2026Article
- Dysregulated m6A RNA methylation in tuberculosis: association with altered methyltransferase expression and immune responses.BMC infectious diseases · 2026Article
- Dual role of miR-21-enriched MSC-derived exosomes in diabetic nephropathy: therapeutic potential versus p53-driven pathogenicity.BMC nephrology · 2026Article
- METTL14 knockdown mitigates HG-induced HK-2 cell apoptosis, inflammation, and ferroptosis by promoting SLC40A1.European journal of medical research · 2026Article
- mFrontiers in immunology · 2026Review
- Exosome-mediated cell-cell communication: a new perspective on the mechanisms and therapeutic potential of diabetic microvascular complications.Frontiers in pharmacology · 2026Review
- Exo-hydrogel therapy: a revolutionary approach to managing diabetic complications.Journal of nanobiotechnology · 2025Review
- Exosomes applications in kidney diseases.Molecular biology reports · 2025Review
- Extracellular Vesicles in Renal Inflammatory Diseases: Revealing Mechanisms of Extracellular Vesicle-Mediated Macrophage Regulation.International journal of molecular sciences · 2025Review
- Oxidative Stress Induced by Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) Dysfunction Aggravates Chronic Inflammation Through the NADAntioxidants (Basel, Switzerland) · 2025Review
- Specificity of endothelial cells in endothelial dysfunction of diabetic kidney disease and their crosstalk with neighboring cells: an updated review.Frontiers in endocrinology · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMethyltransferase 14 (METTL14) mediated N6-methyladenine (m6A) RNA methylation and progestin and AdipoQ receptor family member 3 (PAQR3) are reported to be involved in diabetic nephropathy (DN) progression. Here, we explored whether the effects of PAQR3 on DN was associated with METTL14-induced m6A and their relationship with macrophage-related exosomes in DN progression.
methodsHuman glomerular endothelial cells (GECs) were incubated in high glucose (HG) condition to mimic DN condition in vitro. Exosomes were isolated from M1 macrophages and co-cultured with GECs. qRT-PCR and western blotting detected the levels of genes and proteins. Cell functions were determined using cell counting kit-8 assay and flow cytometry. ELISA analysis detected inflammatory factors, and oxidative stress was evaluated by measuring reactive oxygen species and malondialdehyde. The m6A modification profile was determined by methylated RNA immunoprecipitation assay and the interaction was verified by dual-luciferase reporter assay.
resultsHG elevated PAQR3 expression levels in GECs. PAQR3 silencing reversed HG-induced viability arrest, apoptosis, inflammatory response, and oxidative stress. M1 macrophage co-culture could suppress HG-induced GEC injury. PAQR3 was packaged into M1 macrophage-derived exosomes, and M1 macrophages regulated HG-induced GEC injury by secreting PAQR3 into cells via exosomes. Mechanistically, METTL14 induced PAQR3 m6A modification. METTL14 was enriched in M1 macrophage-derived exosomes. METTL14 knockdown in M1 macrophage-derived exosomes protected GEC from HG-induced viability arrest, apoptosis, inflammation and oxidative stress by regulating PAQR3.
conclusionExosomal METTL14 derived from M1 macrophages promoted HG-induced apoptosis, inflammation and oxidative stress in GECs by mediating PAQR3 m6A modification.
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