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

Abstract

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 lncRNAs in these processes remains a major challenge. This article reviews the mechanisms of lncRNAs related to oxidative stress in several stages of diabetic wound healing and discusses diagnostic and treatment potential of lncRNAs to treat diabetic wounds by improving oxidative stress, as well as the challenges of using lncRNAs for this purpose. It is hoped that these results will provide new targets and strategies for the diagnosis and treatment of impaired wound healing in diabetic patients.

Recent advances of hydrogels as smart dressings for diabetic wounds

“…, with concentrations reaching 10 × 10 −6 to 1000 × 10 −6 M. 33,34 Studies have also indicated a close correlation between long noncoding ribonucleic acid (RNA) and the production of ROS in diabetes. 35 Excessive accumulation of ROS has been proven to induce damage to various cells (such as keratinocytes, fibroblasts, and endothelial cells), impair cell viability, and inhibit functions such as migration and differentiation. 36,37…”

“…31 The concentration of H 2 O 2 in plasma ranges from 1 Â 10 À6 to 8 Â 10 À6 M (average: 3 Â 10 À6 M), and the average concentration of ROS in healthy cells is 1 Â 10 À6 M. 32 However, in diabetic wounds, sustained high blood sugar can lead to excessive accumulation of ROS through various pathways, such as polyol, advanced glycation end-products (AGEs)/receptor for AGEs, hexosamine, protein kinase C, etc., with concentrations reaching 10 Â 10 À6 to 1000 Â 10 À6 M. 33,34 Studies have also indicated a close correlation between long noncoding ribonucleic acid (RNA) and the production of ROS in diabetes. 35 Excessive accumulation of ROS has been proven to induce damage to various cells (such as keratinocytes, fibroblasts, and endothelial cells), impair cell viability, and inhibit functions such as migration and differentiation. 36,37 2.2.3 Associated abnormal inflammation.…”

Bletilla striata Polysaccharide-/Chitosan-Based Self-Healing Hydrogel with Enhanced Photothermal Effect for Rapid Healing of Diabetic Infected Wounds via the Regulation of Microenvironment

“…Persistent hyperglycemic environment promotes the production of ROS, thereby promoting the inflammation cascade reaction and stimulating oxidative stress, thus forming a vicious circle and eventually leading to chronic wounds. 13 Inspired by the antioxidant activity of hydrogels in free-radical scavenging experiments, we further measured their intracellular antioxidant activity using the DCFH-DA probe. As shown in Figure 7f, the quantity and intensity of fluorescence dots significantly increased after LPS stimulation; however, the increment was reduced by the treatment of hydrogel extracts.…”

“…Persistent infection and excessive reactive oxygen species (ROS) resulting from hyperglycemia can exacerbate inflammatory reactions, leading to oxidative damage and impaired immune cell function, ultimately hindering wound healing. , Berberine (BER) is an isoquinoline alkaloid and exhibits a range of pharmacological activities, including antibacterial, anti-inflammatory, antioxidant, and regulation of glucose and lipid metabolism . These properties make it a promising candidate for alleviating inflammation and oxidative stress in DU.…”

Stem Cell-Derived Extracellular Vesicles: Promising Therapeutic Opportunities for Diabetic Wound Healing

“… 42 LncRNAs have regulatory functions in cell proliferation, invasion, metastasis, apoptosis, and immune response, which are accomplished through epigenetic modification, transcriptional regulation, and translational regulation. 43 LncRNAs are inextricably linked to the regulation of cellular functions and critical biological pathways, demonstrating their potential in diabetic wound healing. The overexpression of linc00511 in ADSC-exos demonstrated competency in DFU healing through inducing angiogenesis, which was attributed to suppressing PAQR3-induced Twist1 ubiquitination degradation.…”