ArticleGut microbes2025
Novel role of FTO in regulation of gut-brain communication via
Article in Gut microbes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Nervonic Acid Prevents HFD-Induced Metabolic Dysfunction and Is Associated with Gut Microbiota Remodeling.Metabolites · 2026Article
- N6-methyladenosine (m6A) methylation in adipose tissue: role, regulation, and therapeutic potential.Cellular and molecular life sciences : CMLS · 2026Review
- Role of gut microbiota dysbiosis in podophyllotoxin-induced neurotoxicity in zebrafish: linking purine metabolism to synaptic dysfunction.BMC microbiology · 2026Article
- The gut-brain axis in arsenic-induced toxicity: mechanisms, consequences, and therapeutic perspectives.Metabolic brain disease · 2026Review
- Article
- Crosstalk between gut microbiota and RNA N6-methyladenosine modification in diabetic retinopathy.Frontiers in cell and developmental biology · 2026Review
- The microbiota-gut-brain axis and central nervous system diseases: from mechanisms of pathogenesis to therapeutic strategies.Frontiers in microbiology · 2025Review
- Altered oral microbiomes in patients with prolonged disorders of consciousness.Journal of oral microbiology · 2025Article
Corrections and comments
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fat mass and obesity-associated protein (FTO) is the key demethylase that reverses the abnormally altered N6-methyladenosine (m6A) modification in eukaryotic cells under environmental pollutants exposure. Arsenic is an environmental metalloid and can cause severe symptoms in human mainly through drinking water. However, there is no specific treatment for its toxic effects due to the uncovered mechanisms. We previously revealed that exposure to arsenic increased the level of m6A via down-regulation of FTO, which might serve as a potential target for intervention against arsenic-related disorders. In this study, our results demonstrated that chronic exposure to arsenic significantly disrupted the intestinal barrier and microenvironment. Also, this administration resulted in the enhancement of m6A modification and the reduction of FTO expression in the intestine. By using both CRISPR/Cas9-based FTO knock-in strategy and adeno-associated virus (AAV)-mediated overexpression of FTO in the intestine, we established for the first time that up-regulation of FTO remarkably ameliorated arsenic-induced disruption of intestinal barriers and altered microenvironment of mice. We also firstly identified a dominant gut microbial species,
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.