Abstract:A variety of novel drugs and advanced therapeutic strategies have been developed for diabetic foot ulcers (DFUs); however, the clinical outcomes are unsatisfactory and the underlying mechanisms of DFU remain elusive. MicroRNAs (miRNA) regulate the pathological processes of many diseases. Fibroblasts are involved in each stage of wound healing, and the functions of fibroblasts may be regulated by miRNAs. In the present study, we found that the levels of miRNA-21-3p (miR-21-3p) were decreased in patients with di… Show more
“…This ultimately will inhibit cell apoptosis, improve the level of inflammation, and promote the proliferation, migration, and differentiation of endothelial cells, keratinocytes, and fibroblasts to accelerate the process of angiogenesis, re-epithelialization, and ECM remodeling, which in turn accelerate wound healing ( Figure 5 ). 35 , 49 , 51 , 52 , 56 , 63 , 64 , 65 Figure 5 Regulatory effects of certain common ncRNAs on the pathology of diabetic wounds The diabetic wound microenvironment induces ncRNA changes, which in turn, causes an imbalance in the downstream gene expression, thereby impairing the functions of immune cells, endothelial cells, keratinocytes, and fibroblasts in the wound and causing cytokine imbalance, further exacerbating the diabetic wound. Moreover, these three pathological processes are inter-related.…”
Section: Ncrnamentioning
confidence: 99%
“… in vitro plasmid transfection 95 miR-21 ↓ By activating the Wnt/β-catenin/MMP-7 pathway, miR-21 promotes the proliferation and migration of keratinocytes in vitro and promotes re-epithelialization, collagen remodeling, and angiogenesis in mice to promote diabetic wound healing. type 1 diabetic rats liposome transfection 56 miR-21-3p ↓ directly targets SPRY1 to enhance the function of fibroblasts and increase collagen synthesis, thereby regulating ECM remodeling to speed up the healing of diabetic wounds C57BL/6 mice lipofectamine transfection or direct application of agomiR-21-3p 64 miR-29b ↓ MSCs upregulate miR-29b to target the expression of MMP-9 and increase the expression level of type I collagen to promote wound healing. in vitro MSC transplantation 62 Anti-ECM remodeling miR-378a − Antisense miR-378a promotes angiogenesis by upregulating integrin β-3 and upregulates vimentin to promote the migration and proliferation of fibroblasts to accelerate wound healing.…”
Section: Mirnasmentioning
confidence: 99%
“…This ultimately will inhibit cell apoptosis, improve the level of inflammation, and promote the proliferation, migration, and differentiation of endothelial cells, keratinocytes, and fibroblasts to accelerate the process of angiogenesis, re-epithelialization, and ECM remodeling, which in turn accelerate wound healing (Figure 5). 35,49,51,52,56,[63][64][65] miRNAs The microenvironment of diabetic wounds can induce an imbalance in miRNA expression by affecting the promoter, RNase activity, and methylation process. 20,[22][23][24] Moreover, the abnormally expressed miRNA is involved in various processes of diabetic wound healing, which significantly affects the process of normal wound repair.…”
Section: Introductionmentioning
confidence: 99%
“…miR-21 may regulate fibroblast function through the transforming growth factor (TGF)-b1/NF-kB/miR-21 signaling pathway and play a key role in the healing process of diabetic ulcers 20. In addition, miR-21-3p can also enhance the function of fibroblasts by reducing the expression of its target gene, SPRY1 64. Previous studies have found that microvesicles (MVs) extracted from transfected keratinocytes are rich in miR-21, and direct administration of MVmiR-21 significantly promoted the healing of skin wounds in diabetic rats.…”
Chronic diabetic wounds affect the quality of life of patients, resulting in significant social and economic burdens on both individuals and the health care system. Although treatment methods for chronic diabetic wounds have been explored, there remains a lack of effective treatment strategies; therefore, alternative strategies must be explored. Recently, the abnormal expression of non-coding RNA in diabetic wounds has received widespread attention since it is an important factor in the development of diabetic wounds. This article reviews the regulatory role of three common non-coding RNAs (microRNA [miRNA], long non-coding RNA [lncRNA], and circular RNA [circRNA]) in diabetic wounds and discusses the diagnosis, treatment potential, and challenges of non-coding RNA in diabetic wounds. This article provides insights into new strategies for diabetic wound diagnosis and treatment at the genetic and molecular levels. ncRNA ncRNA refers to a type of RNA that does not encode protein. In the past, it has been shown to participate in a variety of biological processes and play important transcriptional and post-transcriptional regulatory functions. 18 ncRNAs are divided into two categories based on the length of the RNA chain; lncRNA have lengths greater than 200 nucleotides, and small ncRNAs (snRNA) have lengths less than 200 nucleotides. snRNAs can be subdivided into miRNAs and circRNAs. 19 miRNAs inhibit the expression of target genes by binding to the 3 0 untranslated region (3 0 UTR) of the target mRNA. 20 The miRNA gene is processed and cleaved by RNA polymerase II (Pol II) enzyme and endonuclease Drosha III to produce pre-miRNA, which is
“…This ultimately will inhibit cell apoptosis, improve the level of inflammation, and promote the proliferation, migration, and differentiation of endothelial cells, keratinocytes, and fibroblasts to accelerate the process of angiogenesis, re-epithelialization, and ECM remodeling, which in turn accelerate wound healing ( Figure 5 ). 35 , 49 , 51 , 52 , 56 , 63 , 64 , 65 Figure 5 Regulatory effects of certain common ncRNAs on the pathology of diabetic wounds The diabetic wound microenvironment induces ncRNA changes, which in turn, causes an imbalance in the downstream gene expression, thereby impairing the functions of immune cells, endothelial cells, keratinocytes, and fibroblasts in the wound and causing cytokine imbalance, further exacerbating the diabetic wound. Moreover, these three pathological processes are inter-related.…”
Section: Ncrnamentioning
confidence: 99%
“… in vitro plasmid transfection 95 miR-21 ↓ By activating the Wnt/β-catenin/MMP-7 pathway, miR-21 promotes the proliferation and migration of keratinocytes in vitro and promotes re-epithelialization, collagen remodeling, and angiogenesis in mice to promote diabetic wound healing. type 1 diabetic rats liposome transfection 56 miR-21-3p ↓ directly targets SPRY1 to enhance the function of fibroblasts and increase collagen synthesis, thereby regulating ECM remodeling to speed up the healing of diabetic wounds C57BL/6 mice lipofectamine transfection or direct application of agomiR-21-3p 64 miR-29b ↓ MSCs upregulate miR-29b to target the expression of MMP-9 and increase the expression level of type I collagen to promote wound healing. in vitro MSC transplantation 62 Anti-ECM remodeling miR-378a − Antisense miR-378a promotes angiogenesis by upregulating integrin β-3 and upregulates vimentin to promote the migration and proliferation of fibroblasts to accelerate wound healing.…”
Section: Mirnasmentioning
confidence: 99%
“…This ultimately will inhibit cell apoptosis, improve the level of inflammation, and promote the proliferation, migration, and differentiation of endothelial cells, keratinocytes, and fibroblasts to accelerate the process of angiogenesis, re-epithelialization, and ECM remodeling, which in turn accelerate wound healing (Figure 5). 35,49,51,52,56,[63][64][65] miRNAs The microenvironment of diabetic wounds can induce an imbalance in miRNA expression by affecting the promoter, RNase activity, and methylation process. 20,[22][23][24] Moreover, the abnormally expressed miRNA is involved in various processes of diabetic wound healing, which significantly affects the process of normal wound repair.…”
Section: Introductionmentioning
confidence: 99%
“…miR-21 may regulate fibroblast function through the transforming growth factor (TGF)-b1/NF-kB/miR-21 signaling pathway and play a key role in the healing process of diabetic ulcers 20. In addition, miR-21-3p can also enhance the function of fibroblasts by reducing the expression of its target gene, SPRY1 64. Previous studies have found that microvesicles (MVs) extracted from transfected keratinocytes are rich in miR-21, and direct administration of MVmiR-21 significantly promoted the healing of skin wounds in diabetic rats.…”
Chronic diabetic wounds affect the quality of life of patients, resulting in significant social and economic burdens on both individuals and the health care system. Although treatment methods for chronic diabetic wounds have been explored, there remains a lack of effective treatment strategies; therefore, alternative strategies must be explored. Recently, the abnormal expression of non-coding RNA in diabetic wounds has received widespread attention since it is an important factor in the development of diabetic wounds. This article reviews the regulatory role of three common non-coding RNAs (microRNA [miRNA], long non-coding RNA [lncRNA], and circular RNA [circRNA]) in diabetic wounds and discusses the diagnosis, treatment potential, and challenges of non-coding RNA in diabetic wounds. This article provides insights into new strategies for diabetic wound diagnosis and treatment at the genetic and molecular levels. ncRNA ncRNA refers to a type of RNA that does not encode protein. In the past, it has been shown to participate in a variety of biological processes and play important transcriptional and post-transcriptional regulatory functions. 18 ncRNAs are divided into two categories based on the length of the RNA chain; lncRNA have lengths greater than 200 nucleotides, and small ncRNAs (snRNA) have lengths less than 200 nucleotides. snRNAs can be subdivided into miRNAs and circRNAs. 19 miRNAs inhibit the expression of target genes by binding to the 3 0 untranslated region (3 0 UTR) of the target mRNA. 20 The miRNA gene is processed and cleaved by RNA polymerase II (Pol II) enzyme and endonuclease Drosha III to produce pre-miRNA, which is
“…It has been shown to have a role in regulating cell proliferation and apoptosis in diabetic retinopathy and nephropathy [92]. The effects of miR-21 on dysregulated immune response and healing in diabetic wounds have been well characterized [93][94][95]. miR-21 is upregulated during the early phases of diabetic wound healing, and over-expression of miR-21 leads to increased expression of the proinflammatory cytokines IL-1β, TNFα, inducible nitric oxide synthase (iNos), and IL-6 and to the promotion of a pro-inflammatory M1 macrophage phenotype [27].…”
Section: Dysregulated Mirnas In Pressure Ulcer Inflammatory Responsementioning
Pressure ulcers are preventable, yet highly prevalent, chronic wounds that have significant patient morbidity and high healthcare costs. Like other chronic wounds, they are characterized by impaired wound healing due to dysregulated immune processes. This review will highlight key biochemical pathways in the pathogenesis of pressure injury and how this signaling leads to impaired wound healing. This review is the first to comprehensively describe the current literature on microRNA (miRNA, miR) regulation of pressure ulcer pathophysiology.
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