Transforming growth factor‐beta 1, 2, 3 and receptor type I and II in diabetic foot ulcers

Jude, Edward B.; Blakytny, Robert; Bulmer, JN; Boulton, Andrew J.M.; Ferguson, M. W. J.

doi:10.1046/j.1464-5491.2002.00692.x

Cited by 170 publications

(136 citation statements)

References 26 publications

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“…Diabetes may influence foot wound healing in many ways, including an impairment of peripheral circulation, altered leucocyte function, disturbed balance of cytokines and proteases, and even chronic hyperglycaemia itself [78,79,80]. However, until recently, the role of offloading in impaired wound healing has not been considered [81].…”

Section: Wound Healing and The Importance Of Offloadingmentioning

confidence: 99%

“…Recent studies have also demonstrated other abnormalities frequently seen in chronic neuropathic diabetic foot ulcers. Jude et al described the lack of up-regulation of TGF-β1 in foot ulcers, and Lobmann and colleagues described increases in matrix metalloproteinases and decreased concentration of their inhibitors, both of which could explain impaired wound healing [79,80]. A lack of insulin-like growth factor-1 in the basal keratinocyte layer of biopsies from foot ulcers [93], and increased nitric oxide synthase activity in foot ulcers [94] may also be contributory to retarded wound healing in diabetes.…”

Section: Wound Healing and The Importance Of Offloadingmentioning

confidence: 99%

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The diabetic foot: from art to science. The 18th Camillo Golgi lecture

2004

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Diabetic foot ulceration represents a major medical, social and economic problem all over the world. While more than 5% of diabetic patients have a history of foot ulceration, the cumulative lifetime incidence may be as high as 15%. Ethnic differences exist in both ulcer and amputation incidences, with both being less common in patients of Indian subcontinent origin living in the UK. Foot ulceration results from the interaction of several contributory factors, the most important of which is neuropathy. With respect to the management of acute Charcot neuroarthropathy in diabetes, recent studies suggest that bisphosphonates reduce disease activity as judged not only by differences in skin temperature, but also by assessing markers of bone turnover. The use of the total-contact cast is demonstrated in the treatment of acute Charcot feet and of plantar neuropathic ulcers. Histological evidence suggests that pressure relief results in chronic foot ulcers changing their morphological appearance by displaying some features of an acute wound. Thus, repetitive stresses on the insensate foot appear to play a major role in maintaining ulcer chronicity. It is hoped that increasing research activity in foot disease will ultimately result in fewer ulcers and less amputation in diabetes.

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Section: Wound Healing and The Importance Of Offloadingmentioning

confidence: 99%

Section: Wound Healing and The Importance Of Offloadingmentioning

confidence: 99%

The diabetic foot: from art to science. The 18th Camillo Golgi lecture

2004

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“…In 95% of children with atopic dermatitis, specific TGFb1 gene polymorphism coexisted with decreased TGFb1 production [91]. In patients with diabetic foot and leg ulcers due to chronic venous insufficiency, locally reduced levels of TGFb1 and its receptors have been shown [92]. In patients with resistant-to-treatment leg ulcers, a reduced TGFbRII expression in fibroblasts has been demonstrated [93].…”

Section: Tgfb1 In Pathologymentioning

confidence: 99%

Transforming growth factor beta1 (TGFbeta1) in physiology and pathology

Kajdaniuk¹,

Marek²,

Borgiel−Marek³

et al. 2013

Endokrynologia Polska

166

118

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This review describes precisely the consequence of TGFb1 prevalence in the organism, and its significant influence on physiological and pathophysiological processes. Organ and tissue distinctiveness hinder unambiguous characterisation of the cytokine. However, there are constant functions of TGFb1 inducing no controversy: it participates in foetal development, control of cell growth and differentiation, induces fibrosis and scar formation (the process of 'wound healing'), causes the suppression of immune response, is involved in angiogenesis, the development of tumours, and inflammatory processes. Thus, TGFb1 is a multifunctional cytokine. There are three fundamental directions of its activities: I. TGFb1 regulates cell proliferation, growth, differentiation and cells movement. II. TGFb1 has immunomodulatory effects. III. TGFb1 has profibrogenic effects. TGFb1 action can be local and systemic. This review describes TGFb1 in pathology: colitis ulcerosa, Crohn's disease, coeliac disease, diabetic nephropathy, diabetic retinopathy and diabetic foot, pulmonary hypertension, and Alzheimer's disease. TGFb1 and its receptors are also of interest to endocrinologists. Lack of TGFb1-dependent growth control may result in oncogenesis: papillary, follicular and anaplastic thyroid cancers, prostate, breast and uterine cervical cancer, oesophagus, gastric, colorectal and liver cancers, NSCLC, and malignant melanoma. Excessive TGFb1 activity is an integral part of the fibrotic processes occurring in the response to injury. An increased TGFb1 expression has been observed in patients with pulmonary, kidney, and liver fibrosis. In chronic hepatitis, the prolonged stimulation of hepatic stellate cells being the result of chronic damage to hepatocytes results in the release of profibrogenic abundant factors such as TGFb1 and leads to the development of liver cirrhosis. The results of experimental procedures and treatment known as anti-TGFb1 strategy acting against the fibrosis in various tissues leads to hope regarding the use of anti-TGFb1 strategy in clinical practice. StreszczenieW artykule poglądowym szczegółowo opisano konsekwencje rozpowszechnienia TGFb1 w organizmie oraz jego wpływ na szereg procesów fizjologicznych i patofizjologicznych. Istotne odrębności narządowe i tkankowe utrudniają jednoznaczną charakterystykę tej cytokiny. Istnieją jednak stałe funkcje TGFb1 nie wzbudzające kontrowersji: uczestniczy w rozwoju płodu, regulacji wzrostu i różnicowa-nia komórek, indukuje proces włóknienia i bliznowacenia (proces "gojenia rany"), powoduje hamowanie odpowiedzi immunologicznej, uczestniczy w angiogenezie, w rozwoju nowotworów, w procesach zapalnych -jest więc cytokiną wieloczynnościową. Można wyróżnić trzy fundamentalne kierunki jego działania: I -TGFb1 reguluje proliferację, wzrost, różnicowanie i przemieszczanie komórek; II -TGFb1 wykazuje działanie immunomodulujące; III -TGFb1 wykazuje działanie profibrogenne. Działanie TGFb1 może mieć charakter miejscowy i systemowy. Opisano udział TGFb1 w stanach patologicznyc...

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“…Moreover, abnormalities in growth factor expression [45] and other aspects of cell biology have been defined in chronic wounds in diabetes, including changes in the relative concentrations of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) [46]. Neutrophils and macrophages are also known to have impaired function in hyperglycaemia and this could have an adverse impact on healing [47,48].…”

Section: Compressionmentioning

confidence: 99%

A systematic review of the effectiveness of interventions to enhance the healing of chronic ulcers of the foot in diabetes

Hinchliffe

Valk

Apelqvist

et al. 2008

Diabetes Metab. Res. Rev.

204

132

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SummaryThe outcome of management of diabetic foot ulcers is poor and there is uncertainty concerning optimal approaches to management. We have undertaken a systematic review to identify interventions for which there is evidence of effectiveness. A search was made for reports of the effectiveness of interventions assessed in terms of healing, ulcer area or amputation in controlled clinical studies published prior to December 2006. Methodological quality of selected studies was independently assessed by two reviewers using Scottish Intercollegiate Guidelines Network (SIGN) criteria. Selected studies fell into the following categories: sharp debridement and larvae; antiseptics and dressings; chronic wound resection; hyperbaric oxygen (HBO); reduction of tissue oedema; skin grafts; electrical and magnetic stimulation and ultrasound. Heterogeneity of studies prevented pooled analysis of results. Of the 2251 papers identified, 60 were selected for grading following full text review. Some evidence was found to support hydrogels as desloughing agents and to suggest that a systemic (HBO) therapy may be effective. Topical negative pressure (TNP) may promote healing of post-operative wounds, and resection of neuropathic plantar ulcers may be beneficial. More information was needed to confirm the effectiveness and cost-effectiveness of these and other interventions. No data were found to justify the use of any other topically applied product or dressing, including those with antiseptic properties. Further evidence to substantiate the effect of interventions designed to enhance the healing of chronic ulcers is urgently needed. Until such evidence is available from robust trials, there is limited justification for the use of more expensive treatments and dressings.

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Transforming growth factor‐beta 1, 2, 3 and receptor type I and II in diabetic foot ulcers

Abstract: The lack of TGF-beta1 up-regulation in both diabetic foot ulcers and venous ulcers may explain the impaired healing in these chronic wounds, and could represent a general pattern for chronicity.

Cited by 170 publications

References 26 publications

The diabetic foot: from art to science. The 18th Camillo Golgi lecture

The diabetic foot: from art to science. The 18th Camillo Golgi lecture

Transforming growth factor beta1 (TGFbeta1) in physiology and pathology

A systematic review of the effectiveness of interventions to enhance the healing of chronic ulcers of the foot in diabetes

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