晚期糖化终末产物在慢性肾脏病患者肌少症中的作用

O. L. Boriskina, V. N. Tsigan, A. S. Rumyantsev, A. A. Yakovenko
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引用次数: 0

摘要

糖基化终产物(AGEs)的积累与慢性炎症、氧化应激密切相关,并可影响肌肉功能。在已经处于慢性肾病(CKD)形成初期的患者中,可以观察到血清中AGEs浓度的增加。同时,没有必要违反碳水化合物耐受性或糖尿病。肌肉减少症是慢性肾病的并发症之一。它在CKD中的发展不仅可以被认为是内源性中毒的结果,也可以被认为是早衰的一种变体。本文综述了AGEs对CKD骨骼肌减少症发生发展的影响机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of advanced glycation end products in sarcopenia in CKD patients
The accumulation of glycation end products (AGEs) is closely related to chronic inflammation, oxidative stress and can affect muscle function. An increase of the concentration of AGEs in the serum can be observed in patients already at the initial stages of the formation of chronic kidney disease (CKD). At the same time, there is no need for a violation of carbohydrate tolerance or diabetes mellitus. Sarcopenia is one of the complications of CKD. Its development in CKD can be considered not only as a result of endogenous intoxication, but also as one of the variants of premature aging. This literature review is devoted to the analysis of the mechanisms of the influence of AGEs on the occurrence and progression of sarcopenia in CKD.
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