Advanced glycation end products promote ROS production via PKC/p47 phox axis in skeletal muscle cells.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS

ACS Applied Bio Materials Pub Date : 2024-10-05 DOI:10.1186/s12576-024-00944-1

Shinichiro Suzuki, Tatsuya Hayashi, Tatsuro Egawa

引用次数: 0

Abstract

Advanced glycation end products (AGEs) are risk factors for various diseases, including sarcopenia. One of the deleterious effects of AGEs is the induction of abnormal reactive oxygen species (ROS) production in skeletal muscle. However, the underlying mechanism remains poorly understood. Therefore, the aim of this study was to elucidate how AGEs induce ROS production in skeletal muscle cells. This study demonstrated that AGEs treatment promoted ROS production in myoblasts and myotubes while PKC inhibitor abolished ROS production by AGEs stimulation. Phosphorylation of p47 phox by kinases such as PKCα is required to form the Nox2 complex, which induces ROS production. In this study, AGEs treatment promoted the phosphorylation of PKCα and p47 phox in myoblasts and myotubes. Our findings suggest that AGEs promote ROS production through the phosphorylation of PKCα and p47 phox in skeletal muscle cells.

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高级糖化终产物通过 PKC/p47 phox 轴促进骨骼肌细胞产生 ROS。

高级糖化终产物（AGEs）是包括肌肉疏松症在内的多种疾病的危险因素。AGEs 的有害影响之一是诱导骨骼肌产生异常的活性氧（ROS）。然而，人们对其潜在机制仍知之甚少。因此，本研究旨在阐明 AGEs 如何诱导骨骼肌细胞产生 ROS。本研究表明，AGEs 处理可促进肌母细胞和肌管中 ROS 的产生，而 PKC 抑制剂可抑制 AGEs 刺激下的 ROS 产生。p47 phox 被 PKCα 等激酶磷酸化是形成 Nox2 复合物的必要条件，而 Nox2 复合物会诱导 ROS 的产生。在本研究中，AGEs 处理促进了成肌细胞和肌管中 PKCα 和 p47 phox 的磷酸化。我们的研究结果表明，AGEs 可通过磷酸化骨骼肌细胞中的 PKCα 和 p47 phox 促进 ROS 的产生。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464