Long-Term Assessment of Chronic Leg Ulcer Treatment by Autologous Skin Grafts

Ruffieux, P.; Hommel, L.; Saurat, J.‐H.

doi:10.1159/000245698

Cited by 15 publications

(4 citation statements)

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“…There is, as yet, no widely available effective treatment strategy for diabetic foot ulcers. Consequently, novel effective treatment strategies for this chronic complication of diabetes are urgently required ( 4 , 5 ).…”

Section: Introductionmentioning

confidence: 99%

Arnebin-1 promotes angiogenesis by inducing eNOS, VEGF and HIF-1α expression through the PI3K-dependent pathway

Zeng

Huang

Gao

et al. 2015

International Journal of Molecular Medicine

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Arnebin-1, a naphthoquinone derivative, plays a crucial role in the wound healing properties of Zicao (a traditional wound healing herbal medicine). It has been noted that Arnebin-1, in conjunction with vascular endothelial growth factor (VEGF), exerts a synergistic pro-angiogenic effect on human umbilical vein endothelial cells (HUVECs) and accelerates the healing process of diabetic wounds. However, the mechanisms responsible for the pro-angiogenic effect of arnebin-1 on HUVECs and its healing effect on diabetic wounds have not yet been fully elucidated. In this study, in an aim to elucidate these mechanisms of action of arnebin-1, we investigated the effects of arnebin-1 on the VEGF receptor 2 (VEGFR2) and the phosphoinositide 3-kinase (PI3K)-dependent signaling pathways in HUVECs treated with VEGF by western blot analysis. The pro-angiogenic effects of arnebin-1 on HUVECs, including its effects on proliferation and migration, were evaluated by MTT assay, Transwell assay and tube formation assay in vitro. The expression levels of hypoxia-inducible factor (HIF)-1α, endothelial nitric oxide synthase (eNOS) and VEGF were determined by western blot analysis in the HUVECs and wound tissues obtained from non-diabetic and diabetic rats. CD31 expression in the rat wounds was evaluated by immunofluorescence staining. We found that the activation of the VEGFR2 signaling pathway induced by VEGF was enhanced by arnebin-1. Arnebin-1 promoted endothelial cell proliferation, migration and tube formation through the PI3K-dependent pathway. Moreover, Arnebin-1 significantly increased the eNOS, VEGF and HIF-1α expression levels in the HUVECs and accelerated the healing of diabetic wounds through the PI3K-dependent signaling pathway. CD31 expression was markedly enhanced in the wounds of diabetic rats treated with arnebin-1 compared to the wounds of untreated diabetic rats. Therefore, the findings of the present study indicate that arnebin-1 promotes the wound healing process in diabetic rats by eliciting a pro-angiogenic response.

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Section: Introductionmentioning

confidence: 99%

Arnebin-1 promotes angiogenesis by inducing eNOS, VEGF and HIF-1α expression through the PI3K-dependent pathway

Zeng

Huang

Gao

et al. 2015

International Journal of Molecular Medicine

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“…With adequate treatment, some ulcers may last only weeks; however, many ulcers are difficult to treat and may last months, in certain cases years, 19–35% of foot ulcers are reported as nonhealing [5, 6]. Therefore, it is a high priority to develop new strategies for treatment of this devastating complication [7, 8]. Important factors in the healing process include not only macrocirculation, but, more specifically, the local skin microcirculation and oxygenation of the tissue surrounding the ulcer.…”

Section: Introductionmentioning

confidence: 99%

Dipeptidyl Peptidase 4 Inhibition May Facilitate Healing of Chronic Foot Ulcers in Patients with Type 2 Diabetes

Marfella

Sasso

Rizzo

et al. 2012

Experimental Diabetes Research

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The pathophysiology of chronic diabetic ulcers is complex and still incompletely understood, both micro- and macroangiopathy strongly contribute to the development and delayed healing of diabetic wounds, through an impaired tissue feeding and response to ischemia. With adequate treatment, some ulcers may last only weeks; however, many ulcers are difficult to treat and may last months, in certain cases years; 19–35% of ulcers are reported as nonhealing. As no efficient therapy is available, it is a high priority to develop new strategies for treatment of this devastating complication. Because experimental and pathological studies suggest that incretin hormone glucagon-like peptide-1 may improves VEGF generation and promote the upregulation of HIF-1α through a reduction of oxidative stress, the study evaluated the effect of the augmentation of GLP-1, by inhibitors of the dipeptidyl peptidase-4, such as vildagliptin, on angiogenesis process and wound healing in diabetic chronic ulcers. Although elucidation of the pathophysiologic importance of these aspects awaits further confirmations, the present study evidences an additional aspect of how DPP-4 inhibition might contribute to improved ulcer outcome.

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“…Angioplasty or bypass surgery is generally ineffective in small-vessel disease and amputation becomes inevitable due to persistent critical limb ischemia, soft-tissue infection, and impaired wound healing with osteomyelitis [13,14]. Skin grafts with different techniques are performed with the intention to heal the ulcers in selected cases [15]. Many adjunctive therapies are designed for the care of chronic diabetic foot ulcers including hyperbaric oxygen therapy (HBO), ultrasound, recombinant human platelet-derived growth factor-BB, vacuum-assisted wound closure, and acellular matrix with HBO being the most commonly used [13, 16 -22].…”

Section: Introductionmentioning

confidence: 99%