RNA N6-methyladenosine demethylase FTO promotes diabetic wound healing through TRIB3-mediated autophagy in an m6A-YTHDF2-dependent manner
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| Publicado no: | Cell Death and Disease vol. 16, no. 1 (Dec 2025), p. 222 |
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| Publicado em: |
Springer Nature B.V.
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| Assuntos: | |
| Acesso em linha: | Citation/Abstract Full Text - PDF |
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MARC
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| 022 | |a 2041-4889 | ||
| 024 | 7 | |a 10.1038/s41419-025-07494-3 |2 doi | |
| 035 | |a 3182928474 | ||
| 045 | 2 | |b d20251201 |b d20251231 | |
| 084 | |a 274832 |2 nlm | ||
| 245 | 1 | |a RNA N<sup>6</sup>-methyladenosine demethylase FTO promotes diabetic wound healing through TRIB3-mediated autophagy in an m<sup>6</sup>A-YTHDF2-dependent manner | |
| 260 | |b Springer Nature B.V. |c Dec 2025 | ||
| 513 | |a Journal Article | ||
| 520 | 3 | |a N6-methyladenosine (m6A) RNA modification impaired autophagy results in delayed diabetic wound healing. In this study, it was found that fat mass and obesity-associated protein (FTO) was significantly downregulated in the epidermis of diabetic patients, STZ-induced mice and db/db mice (type I and II diabetic mice) with prolonged hyperglycemia, as well as in different types of keratinocyte cell lines treated with short-term high glucose medium. The knockout of FTO affected the biological functions of keratinocytes, including enhanced apoptosis, inhibited autophagy, and delayed wound healing, producing consistent results with high-glucose medium treatment. High-throughput analysis revealed that tribbles pseudokinase 3 (TRIB3) served as the downstream target gene of FTO. In addition, both in vitro and in vivo experiments, TRIB3 overexpression partially rescued biological functions caused by FTO-depletion, promoting keratinocyte migration and proliferation via autophagy. Epigenetically, FTO modulated m6A modification in the 3’UTR of TRIB3 mRNA and enhanced TRIB3 stability in a YTHDF2-dependent manner. Collectively, this study identifies FTO as an accelerator of diabetic wound healing and modulates autophagy via regulating TRIB3 in keratinocytes, thereby benefiting the development of a m6A-targeted therapy for refractory diabetic wounds. | |
| 653 | |a Diabetes | ||
| 653 | |a Keratinocytes | ||
| 653 | |a 3' Untranslated regions | ||
| 653 | |a Autophagy | ||
| 653 | |a N6-methyladenosine | ||
| 653 | |a Apoptosis | ||
| 653 | |a Wound healing | ||
| 653 | |a Hyperglycemia | ||
| 653 | |a Cell lines | ||
| 653 | |a mRNA stability | ||
| 653 | |a Diabetes mellitus | ||
| 653 | |a RNA modification | ||
| 653 | |a Epidermis | ||
| 653 | |a Body fat | ||
| 773 | 0 | |t Cell Death and Disease |g vol. 16, no. 1 (Dec 2025), p. 222 | |
| 786 | 0 | |d ProQuest |t Science Database | |
| 856 | 4 | 1 | |3 Citation/Abstract |u https://www.proquest.com/docview/3182928474/abstract/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch |
| 856 | 4 | 0 | |3 Full Text - PDF |u https://www.proquest.com/docview/3182928474/fulltextPDF/embedded/7BTGNMKEMPT1V9Z2?source=fedsrch |