Roxadustat promotes angiogenesis through HIF‐1α/VEGF/VEGFR2 signaling and accelerates cutaneous wound healing in diabetic rats.

Diabetic foot ulcers are a major health‐care burden worldwide. One primary cause of the delayed wound healing in diabetic patients is impaired function of the hypoxia‐inducible factor‐1α/vascular endothelial growth factor (HIF‐1α/VEGF) axis, which results in compromised neovascularization in respons...

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Publicado en:Wound Repair & Regeneration Vol. 27; no. 4; pp. 324 - 335
Autores principales: Zhu, Yu, Wang, Yanmao, Jia, Yachao, Xu, Jia, Chai, Yimin
Formato: pictorial research tables/charts Journal Article
Publicado: Wiley-Blackwell Jul2019
Acceso en línea:Ver este registro en EBSCOhost
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        atl: Roxadustat promotes angiogenesis through HIF‐1α/VEGF/VEGFR2 signaling and accelerates cutaneous wound healing in diabetic rats.
      aug:
        au:
          Zhu, Yu
          Wang, Yanmao
          Jia, Yachao
          Xu, Jia
          Chai, Yimin
        affil: Department of Orthopedic Surgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Yishan Rd 600, Shanghai 200233 PR China
      sug:
        subj:
          Enzyme Inhibitors Pharmacodynamics
          Neovascularization, Physiologic Drug Effects
          DNA-Binding Proteins Drug Effects
          Vascular Endothelial Growth Factors Drug Effects
          Signal Transduction Drug Effects
          Wound Healing Drug Effects
          Skin Physiology Drug Effects
          Diabetes Mellitus Chemically Induced
          Animal Studies
          Rats
          Umbilical Veins Drug Effects
          Epithelium Drug Effects
          In Vivo Studies
          Biological Assay Methods
          Urea Adverse Effects
      ab: Diabetic foot ulcers are a major health‐care burden worldwide. One primary cause of the delayed wound healing in diabetic patients is impaired function of the hypoxia‐inducible factor‐1α/vascular endothelial growth factor (HIF‐1α/VEGF) axis, which results in compromised neovascularization in response to hypoxia. In the present study, we aimed to investigate the effect of roxadustat, a novel HIF prolyl‐4‐hydroxylase inhibitor, on angiogenesis and its therapeutic effect on cutaneous wound healing in diabetic rats. In vitro, we found that roxadustat could promote the angiogenic activity of human umbilical vein endothelial cells, accompanied by up‐regulation of HIF‐1α/VEGF/VEGFR2 signaling. Next, we demonstrated that Ki8751, a VEGFR2‐specific inhibitor, could inhibit the increased angiogenic activity of human umbilical vein endothelial cells induced by roxadustat. In vivo, we performed a Matrigel plug assay and demonstrated that roxadustat induced vascularization of the Matrigel plugs, and this effect could be partially inhibited by Ki8751. Finally, we utilized a streptozotocin‐induced diabetic rat model and found that roxadustat could accelerate cutaneous wound healing and promote angiogenesis in the wound sites. In conclusion, roxadustat promotes angiogenesis via activation of the HIF‐1α/VEGF/VEGFR2 pathway and exhibits therapeutic effects on diabetic wound healing by increasing angiogenesis. Our findings suggest that roxadustat can be a promising strategy to promote diabetic cutaneous wound healing.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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