ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
m6A demethylase Fto inhibited macrophage activation and glycolysis in diabetic nephropathy via m6A/Npas2/Hif-1α axis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Natural products modulate renal metabolic reprogramming in diabetic kidney disease.Journal of translational internal medicine · 2026Article
- Mitochondrial metabolic reprogramming drives diabetic kidney disease progression: cell-specific mechanisms, metabolic memory, and targeted strategies.Molecular medicine (Cambridge, Mass.) · 2026Review
- The translational potential of m6A RNA methylation in DKD: emerging biomarkers for early detection and targeted therapies.Frontiers in medicine · 2026Review
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
- The gut-joint axis in gout: microbial outer membrane vesicles and mFrontiers in immunology · 2026Review
- RNA epitranscriptomic regulation of tumor immune evasion: mechanisms, context-dependent roles, and therapeutic implications.Frontiers in immunology · 2026Review
- Therapy-induced mRNA, rRNA and tRNA methylation alterations confer tolerance phenotype in tumor cells: mechanism and implications.International journal of biological sciences · 2026Review
- Mitochondria at the intersections of RNA modifications and metabolism reprogramming implications in cell death, tumor microenvironment, and immunotherapy.Journal of hematology & oncology · 2025Review
- Mechanisms of gypenosides in type 2 diabetes mellitus via regulation of m6A methylase METTL3/14 and demethylase FTO.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- Decoding mJournal of translational medicine · 2025Review
- The crucial role of metabolic reprogramming in driving macrophage conversion in kidney disease.Cellular & molecular biology letters · 2025Review
- FTO controls CD8Cell death & disease · 2025Article
- m6A demethylase Fto inhibited macrophage activation and glycolysis in diabetic nephropathy via m6A/Npas2/Hif-1α axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The latest progression of N6-methyladenosine (mFrontiers in endocrinology · 2025Review
- mKidney diseases (Basel, Switzerland)Article
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9 authors.
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Abstract
Macrophage infiltration and activation is a key factor in the progression of diabetic nephropathy (DN). However, aerobic glycolysis induced by m6A methylation modification plays a key role in M1-type activation of macrophages, but the specific mechanism remains unclear in DN. In this study, the expression of m6A demethylase Fto in bone marrow derived macrophages and primary kidney macrophages from db/db mice. Loss and gain-of-function analysis of Fto were performed to assess the role of Fto in DN. Transcriptome and MeRIP-seq association analysis was performed to identified the target gene was Npas2. In this study, we found that demethylase Fto exhibits low expression in type 2 DN m6A modification of Npas2 mediated by Fto regulates macrophages M1-type activation and glucose metabolism reprogramming to participate in the process of DN. Furthermore, Fto reduces the m6A modification level of Npas2 in macrophages through a Prrc2a-dependent mechanism, and decreasing its stability. This process mediates inflammation and glycolysis in M1 macrophages by regulating the Hif-1α signaling pathway. Fto may act as a suppressor of M1 macrophages inflammation and glycolysis in DN through the m6A/Npas2/Hif-1α axis. This findings providing a new basis for the prevention and treatment of DN.
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