FTO Modulates m 6 A RNA Methylation of STC1 to Regulate Inflammation and Oxidative Stress in Diabetic Nephropathy
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Le résumé fourni par la source
ABSTRACT Diabetic nephropathy (DN) is a major cause of chronic kidney disease, driven by hyperglycemia‐induced kidney damage. Recently research has highlighted the role of N6‐methyladenosine (m 6 A) RNA methylation in the progression of DN. The role of the fat mass and obesity‐associated protein (FTO), an essential m 6 A demethylase, in DN remains uncertain despite its association with various diseases. Datasets (GSE96804 and GSE30528) were used to identify differentially expressed genes in DN. Diabetic cell models were established by culturing human renal glomerular endothelial cells (HRGECs) and mesangial cells (HRMCs) in high glucose conditions. FTO expression was manipulated through overexpression and knockdown, and its effects on cell viability, apoptosis, ROS production, inflammatory factor secretion, and m 6 A modifications were assessed. In vivo, db/db mice were used to evaluate the therapeutic potential of FTO and stanniocalcin‐1 (STC1) gene modulation. FTO was significantly downregulated in DN models, and overexpression of FTO in HRGECs under high glucose conditions alleviated oxidative stress, reduced inflammation, and improved cell viability. LSP1P5 and STC1 were identified as potential downstream targets of FTO, with m 6 A methylation levels of STC1 significantly altered by FTO modulation. In vivo, FTO overexpression improved kidney function and mitigated inflammation and oxidative stress, whereas STC1 exacerbated kidney injury, indicating a complex interplay between FTO and STC1 in DN progression. This study demonstrates that FTO modulates m 6 A RNA methylation of STC1 to regulate inflammation and oxidative stress in DN. Targeting the FTO/STC1 axis may offer a novel therapeutic strategy for managing DN and preventing kidney damage.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé, mais le titre doit être comparé manuellement.
- Titre Crossref
- <scp>FTO</scp> Modulates <scp> m <sup>6</sup> A RNA </scp> Methylation of <scp>STC1</scp> to Regulate Inflammation and Oxidative Stress in Diabetic Nephropathy
- Date Crossref
- 03/12/2025
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Zhengzhou University Research Institute of Nephrology pays non établi dans la noticeUniversité ou école supérieure
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First Affiliated Hospital of Henan University of Traditional Chinese Medicine pays non établi dans la noticeÉtablissement de santé
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First Affiliated Hospital of Zhengzhou University pays non établi dans la noticeÉtablissement de santé
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Henan Provincial Center for Disease Control and Prevention pays non établi dans la noticeOrganisme public
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Henan Province Research Center for Kidney Disease Zhengzhou P. R. China pays non établi dans la noticeStructure de recherche
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Key Laboratory of Precision Diagnosis and Treatment for Chronic Kidney Disease in Henan Province Zhengzhou P. R. China pays non établi dans la noticeStructure de recherche
Research Institute of Nephrology — Zhengzhou University, First Affiliated Hospital of Henan University of Traditional Chinese Medicine et First Affiliated Hospital of Zhengzhou University, avec 3 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.