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晚期糖基化终末产物与糖尿病伤口愈合受损

Advanced glycoxidation products and impaired diabetic wound healing.

作者信息

Peppa Melpomeni, Stavroulakis Panagiotis, Raptis Sotirios A

机构信息

Endocrine Unit, Second Department of Internal Medicine-Propaedeutic, Research Institute and Diabetes Center, Athens University Medical School, Attikon University Hospital, Athens, Greece.

出版信息

Wound Repair Regen. 2009 Jul-Aug;17(4):461-72. doi: 10.1111/j.1524-475X.2009.00518.x.

Abstract

Impaired wound healing is an important diabetic complication associated with increased morbidity and mortality. It appears to be the net result of micro- and macrovascular disease. Diabetic neuropathy and the resulting loss of protective sensation (LOPS) has been recognized as one of the major causes for delayed healing in diabetic foot ulcer patients. In addition, hyperglycemia and a number of hyperglycemia-related factors have been linked to impaired diabetic wound healing, including advanced glycation end products (AGE). A large body of evidence from in vitro and in vivo studies and also data from studies using anti-AGE agents, indicate that AGE may play a role in the pathogenesis of impaired diabetic wound healing. AGE affect the wound healing process either directly by their interference with a variety of components involved or indirectly through their association with diabetic neuropathy and/or angiopathy. However, further studies need to be performed, mostly clinical studies, to evaluate the exact role of AGE in the impaired diabetic wound healing, suggesting new therapeutic approaches.

摘要

伤口愈合受损是一种重要的糖尿病并发症,与发病率和死亡率增加相关。它似乎是微血管和大血管疾病的最终结果。糖尿病神经病变及由此导致的保护性感觉丧失(LOPS)已被认为是糖尿病足溃疡患者伤口愈合延迟的主要原因之一。此外,高血糖及一些与高血糖相关的因素与糖尿病伤口愈合受损有关,包括晚期糖基化终产物(AGE)。大量体外和体内研究的证据以及使用抗AGE药物的研究数据表明,AGE可能在糖尿病伤口愈合受损的发病机制中起作用。AGE通过干扰多种相关成分直接影响伤口愈合过程,或通过与糖尿病神经病变和/或血管病变相关间接影响伤口愈合过程。然而,需要进行更多研究,主要是临床研究,以评估AGE在糖尿病伤口愈合受损中的确切作用,从而提出新的治疗方法。

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