LncRNAs associated with oxidative stress in diabetic wound healing: Regulatory mechanisms and application prospects

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Diabetes is a group of chronic diseases with blood glucose imbalance, and long-term hyperglycaemia causes sustained damage to various organs of the body, resulting in vascular lesions, neuropathy and impaired wound healing. Diabetic wound formation involves a variety of complex mechanisms, and they are characterized by a persistent chronic inflammatory response, degradation of angiogenesis and imbalance of extracellular matrix regulation, all of which are related to oxidative stress. Additionally, repair and healing of diabetic wounds require the participation of a variety of cells, cytokines, genes, and other factors, which together constitute a complex biological regulatory network. Recent studies have shown that long noncoding RNAs (lncRNAs) can be involved in the regulation of several key biological pathways and cellular functions demonstrating their critical role in diabetic wound healing. LncRNAs are a major family of RNAs with limited or no protein-coding function. Numerous studies have recently reported a strong link between oxidative stress and lncRNAs. Given that both lncRNAs and oxidative stress have been identified as potential drivers of diabetic wound healing, their link in diabetic wound healing can be inferred. However, the specific mechanism of oxidative stress related to lncRNAs in diabetic wound healing is still unclear, and elucidating the functions of lncRN

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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