
Research Square (Research Square), Год журнала: 2024, Номер unknown
Опубликована: Дек. 11, 2024
Язык: Английский
Research Square (Research Square), Год журнала: 2024, Номер unknown
Опубликована: Дек. 11, 2024
Язык: Английский
Functional & Integrative Genomics, Год журнала: 2025, Номер 25(1)
Опубликована: Май 24, 2025
Emerging evidence supports that angiogenesis is essential for the wound healing of diabetic foot ulcer (DFU), and high glucose (HG)-induced dysfunction human dermal microvascular endothelial cells a key factor hinders angiogenesis. However, underlying mechanisms by which HG leads to has not been fully elucidated. In present investigation, we discovered significant upregulation long non-coding RNA GFOD1-AS1(GFOD1-AS1) in margin samples patients with DFU HG-induced model cells, attributing its dysregulation stabilizing effect NAT10-mediated ac4C modification, as corroborated an integrated approach data mining experimental validation. Subsequently, series vitro functional analyses showed ectopic expression GFOD1-AS1 promoted impaired function cells. contrast, knockdown significantly alleviated impairment indicated enhanced cell proliferation, migration, tube formation. Mechanistically, directly interacts DNA methyltransferase DNMT1 block ubiquitin-proteasome degradation, thereby enhancing protein stability DNMT1.This elevates expression, ultimately inducing summary, our results reveal serves potential therapeutic target DFU, highlight critical role NAT10/GFOD1-AS1/DNMT1 axis DFU.
Язык: Английский
Процитировано
0Research Square (Research Square), Год журнала: 2024, Номер unknown
Опубликована: Дек. 11, 2024
Язык: Английский
Процитировано
0