阻断mini- trpr治疗糖尿病足综合征

E. Biros, V. Vangaveti, C. Moran, U. Malabu
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引用次数: 0

摘要

糖尿病足综合征表现出由于下肢组织灌注受损而导致的伤口慢性。先前的研究表明,干扰素-γ (IFN-γ)是糖尿病足综合征的一种中枢炎症介质,可诱导截断形式的色氨酸- trna合成酶(mini- trpr),该酶具有很强的血管抑制特性。最近,我们报道了在体外用d -色氨酸阻断IFN-γ存在的mini-TrpRS信号传导。在这里,我们讨论了IFN-γ/mini-TrpRS轴在糖尿病足综合征的病理和新兴的治疗方案。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Blockade of mini-TrpRS for treatment of diabetic foot syndrome
Diabetic foot syndrome demonstrates wound chronicity due to impaired tissue perfusion in lower limbs. Previous studies showed interferon-gamma (IFN-γ), a central inflammatory mediator in diabetic foot syndrome, to induce the truncated form of tryptophanyl-tRNA synthetase (mini-TrpRS) that has strong angiostatic properties. Recently we reported that mini-TrpRS signalling could be blocked in the presence of IFN-γ with D-tryptophan in vitro. Here we discuss the IFN-γ/mini-TrpRS axis in the pathology of diabetic foot syndrome and emerging therapeutic options.
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