Expression of miR-217 and HIF-1α/VEGF pathway in patients with diabetic foot ulcer and its effect on angiogenesis of diabetic foot ulcer rats

Lin, Chujia; Lan, Yong; Ou, Meng; Ji, Leiquan; Lin, Shaoda

doi:10.1007/s40618-019-01053-2

Cited by 79 publications

(54 citation statements)

References 52 publications

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“…HIF-1α, a known target of miR-217, regulates a series of genes including VEGF, as well as pathways involved in angiogenesis. Serum miR-217 is increased in diabetic patients, and even more so in diabetic patients suffering from DFUs [ 203 ]. When miR-127 inhibitors were applied to wounds, angiogenic activities were improved through the elevated HIF-1α expression and regulation of the VEGF pathway, in rodents [ 203 ].…”

Section: Circulating and Tissue Micrornas As Biomarkers For The Eamentioning

confidence: 99%

Mechanistic Actions of microRNAs in Diabetic Wound Healing

Petković

Sørensen

Leal

et al. 2020

Cells

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Wound healing is a complex biological process that is impaired under diabetes conditions. Chronic non-healing wounds in diabetes are some of the most expensive healthcare expenditures worldwide. Early diagnosis and efficacious treatment strategies are needed. microRNAs (miRNAs), a class of 18–25 nucleotide long RNAs, are important regulatory molecules involved in gene expression regulation and in the repression of translation, controlling protein expression in health and disease. Recently, miRNAs have emerged as critical players in impaired wound healing and could be targets for potential therapies for non-healing wounds. Here, we review and discuss the mechanistic background of miRNA actions in chronic wounds that can shed the light on their utilization as specific wound healing biomarkers.

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Section: Circulating and Tissue Micrornas As Biomarkers For The Eamentioning

confidence: 99%

Mechanistic Actions of microRNAs in Diabetic Wound Healing

Petković

Sørensen

Leal

et al. 2020

Cells

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“…The present study observed that miR-217 was a target of hsa_circ_0058092. It has been demonstrated that miR-217 serum levels are upregulated in patients with diabetic foot ulcers when compared to healthy controls ( 31 ). The suppression of miR-217 protects against HG-induced podocyte injury and insulin resistance by restoring phosphatase and tensin homologue-mediated autophagy pathways ( 32 ).…”

Section: Discussionmentioning

confidence: 99%

hsa_circ_0058092 protects against hyperglycemia‑induced endothelial progenitor cell damage via miR‑217/FOXO3

Cheng

Zheng

et al. 2020

Int J Mol Med

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Circular RNAs (circRNAs) regulate the expression of genes that are critical for various biological and pathological processes. Previous studies have reported that the expression of hsa_circ_0058092 is decreased in patients with diabetes mellitus (DM); however, the specific role of this circRNA in DM is unknown. In the present study, endothelial progenitor cells (EPCs) were isolated and a decreased hsa_circ_0058092 expression was found under conditions of hyperglycemia (HG). The overexpression of hsa_circ_0058092 protected the EPCs against HG-induced damage by preserving cell survival, proliferation, migration and angiogenic differentiation. The overexpression of hsa_circ_0058092 also decreased the HG-induced increase in NADPH-oxidase proteins and inflammatory cytokines. Further investigation revealed that the overexpression of hsa_circ_0058092 enhanced FOXO3 expression, which was mediated through the interaction with miR-217. Furthermore, the upregulation of miR-217 or the downregulation of FOXO3 abolished the protective effects of hsa_circ_0058092 against HG-induced EPC damage. On the whole, these data suggest that hsa_circ_0058092 acts via the miR-217/FOXO3 pathway to protect against EPCs HG-induced damage, and to preserve the migration and angiogenesis of EPCs.

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“…One reason for this is that neovessels deliver oxygen and nutrients to promote new tissue formation during the proliferative phase of healing [15]. Diabetic wounds exhibit decreased capillary density and vascularity due to insufficient angiogenesis [15,16]. Specifically, it has been shown that in chronic diabetic wounds, the angiogenic response normally induced by hypoxia is dysregulated [15,17].…”

Section: Wound Healingmentioning

confidence: 99%

The Role of High-Density Lipoproteins in Endothelial Cell Metabolism and Diabetes-Impaired Angiogenesis

Primer

Psaltis

Tan

et al. 2020

IJMS

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Diabetes mellitus affects millions of people worldwide and is associated with devastating vascular complications. A number of these complications, such as impaired wound healing and poor coronary collateral circulation, are characterised by impaired ischaemia-driven angiogenesis. There is increasing evidence that high-density lipoproteins (HDL) can rescue diabetes-impaired angiogenesis through a number of mechanisms, including the modulation of endothelial cell metabolic reprogramming. Endothelial cell metabolic reprogramming in response to tissue ischaemia is a driver of angiogenesis and is dysregulated by diabetes. Specifically, diabetes impairs pathways that allow endothelial cells to upregulate glycolysis in response to hypoxia adequately and impairs suppression of mitochondrial respiration. HDL rescues the impairment of the central hypoxia signalling pathway, which regulates these metabolic changes, and this may underpin several of its known pro-angiogenic effects. This review discusses the current understanding of endothelial cell metabolism and how diabetes leads to its dysregulation whilst examining the various positive effects of HDL on endothelial cell function.

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Expression of miR-217 and HIF-1α/VEGF pathway in patients with diabetic foot ulcer and its effect on angiogenesis of diabetic foot ulcer rats

Cited by 79 publications

References 52 publications

Mechanistic Actions of microRNAs in Diabetic Wound Healing

Mechanistic Actions of microRNAs in Diabetic Wound Healing

hsa_circ_0058092 protects against hyperglycemia‑induced endothelial progenitor cell damage via miR‑217/FOXO3

The Role of High-Density Lipoproteins in Endothelial Cell Metabolism and Diabetes-Impaired Angiogenesis

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