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

IF 2.6 4区 医学 Q2 PHYSIOLOGY Journal of Physiological Sciences Pub Date : 2024-10-05 DOI:10.1186/s12576-024-00944-1
Shinichiro Suzuki, Tatsuya Hayashi, Tatsuro Egawa
{"title":"Advanced glycation end products promote ROS production via PKC/p47 phox axis in skeletal muscle cells.","authors":"Shinichiro Suzuki, Tatsuya Hayashi, Tatsuro Egawa","doi":"10.1186/s12576-024-00944-1","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":16832,"journal":{"name":"Journal of Physiological Sciences","volume":"74 1","pages":"51"},"PeriodicalIF":2.6000,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11452979/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Physiological Sciences","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12576-024-00944-1","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
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.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
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。
求助全文
约1分钟内获得全文 去求助
来源期刊
CiteScore
4.40
自引率
4.30%
发文量
27
审稿时长
6-12 weeks
期刊介绍: The Journal of Physiological Sciences publishes peer-reviewed original papers, reviews, short communications, technical notes, and letters to the editor, based on the principles and theories of modern physiology and addressed to the international scientific community. All fields of physiology are covered, encompassing molecular, cellular and systems physiology. The emphasis is on human and vertebrate physiology, but comparative papers are also considered. The process of obtaining results must be ethically sound. Fields covered: Adaptation and environment Autonomic nervous function Biophysics Cell sensors and signaling Central nervous system and brain sciences Endocrinology and metabolism Excitable membranes and neural cell physiology Exercise physiology Gastrointestinal and kidney physiology Heart and circulatory physiology Molecular and cellular physiology Muscle physiology Physiome/systems biology Respiration physiology Senses.
期刊最新文献
Effects of systemic ventricular assist in failing Fontan patients: a theoretical analysis using a computational model. ADAM8 promotes alcoholic liver fibrosis through the MAPK signaling pathway. Advanced glycation end products promote ROS production via PKC/p47 phox axis in skeletal muscle cells. Acupuncture improves spatial learning and memory impairment caused by herpes simplex virus type-1 in rats through the p38 MAPK/CREB pathway. Thermosensing ability of TRPC5: current knowledge and unsettled questions.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1