The possible role of tumor necrosis factor-alpha in diabetic polyneuropathy.

Jo Satoh, Soroku Yagihashi, Takayoshi Toyota
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引用次数: 119

Abstract

In this review, the authors provide evidences that imply the role of tumor necrosis factor-alpha (TNF-alpha) in the pathogenesis of diabetic complications, especially diabetic polyneuropathy. Under chronic hyperglycemia, endogenous TNF-alpha production is accelerated in microvascular and neural tissues, which may undergo an increased microvascular permeability, hypercoagulability, and nerve damage, thus initiating and promoting the development of characteristic lesions of diabetic microangiopathy and polyneuropathy. Enhanced TNF-alpha production may also promote atherosclerosis due to increased insulin resistance and the expression of adhesion molecules. Clinical application of specific agents that suppress production and/or activity of TNF-alpha may inhibit the development and exacerbation of chronic diabetic complications.

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肿瘤坏死因子- α在糖尿病多发性神经病中的可能作用。
本文综述了肿瘤坏死因子- α (tnf - α)在糖尿病并发症,特别是糖尿病多发性神经病变发病机制中的作用。慢性高血糖时,微血管和神经组织内源性tnf - α生成加速,微血管通透性增加,高凝性增加,神经损伤,从而引发和促进糖尿病微血管病变和多发性神经病变特征性病变的发展。由于胰岛素抵抗和粘附分子的表达增加,tnf - α的产生增强也可能促进动脉粥样硬化。临床应用特异性药物抑制tnf - α的产生和/或活性可能抑制慢性糖尿病并发症的发展和恶化。
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Acknowledgment to Reviewers Glucose intolerance and hyperlipidemia prior to diabetes onset in female Spontaneously Diabetic Torii (SDT) rats. Role of glucose in IRS signaling in rat pancreatic islets: specific effects and interplay with insulin. Fructose diet-induced skin collagen abnormalities are prevented by lipoic acid. Pentoxifylline diminishes the oxidative damage to renal tissue induced by streptozotocin in the rat.
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