Does the insulin-like growth factor system interact with prostaglandins and proinflammatory cytokines during neurodegeneration?

B. Lackey, S. L. Gray, D. Henricks
{"title":"Does the insulin-like growth factor system interact with prostaglandins and proinflammatory cytokines during neurodegeneration?","authors":"B. Lackey, S. L. Gray, D. Henricks","doi":"10.1111/J.1525-1373.2000.22360.X","DOIUrl":null,"url":null,"abstract":"Prostaglandins and proinflammatory cytokines are implicated in the etiology of neurodegenerative diseases, such as Alzheimer's disease. Signaling cascades initiated by these factors may result in reactive oxygen species generation and cell death. The insulin-like growth factors (IGF) are ubiquitous polypeptides involved in all aspects of growth and development. Additionally, the IGF are regarded as survival factors that display potent antiapoptotic activity. Interfering with IGF production, distribution, or signaling may result in greater susceptibility to apoptotic stimuli. In neurodegenerative conditions, the IGF appear to be antagonized by prostaglandins and proinflammatory cytokines. In this review, the relationship among specific prostaglandins, the proinflammatory factors, tumor necrosis factor, interleukin-1, and interleukin-6, and the IGF system will be investigated.","PeriodicalId":20618,"journal":{"name":"Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine","volume":"56 4 1","pages":"20-7"},"PeriodicalIF":0.0000,"publicationDate":"2000-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"9","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1111/J.1525-1373.2000.22360.X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 9

Abstract

Prostaglandins and proinflammatory cytokines are implicated in the etiology of neurodegenerative diseases, such as Alzheimer's disease. Signaling cascades initiated by these factors may result in reactive oxygen species generation and cell death. The insulin-like growth factors (IGF) are ubiquitous polypeptides involved in all aspects of growth and development. Additionally, the IGF are regarded as survival factors that display potent antiapoptotic activity. Interfering with IGF production, distribution, or signaling may result in greater susceptibility to apoptotic stimuli. In neurodegenerative conditions, the IGF appear to be antagonized by prostaglandins and proinflammatory cytokines. In this review, the relationship among specific prostaglandins, the proinflammatory factors, tumor necrosis factor, interleukin-1, and interleukin-6, and the IGF system will be investigated.
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
在神经退行性变过程中,胰岛素样生长因子系统是否与前列腺素和促炎细胞因子相互作用?
前列腺素和促炎细胞因子与神经退行性疾病的病因有关,如阿尔茨海默病。这些因素引发的信号级联反应可能导致活性氧的产生和细胞死亡。胰岛素样生长因子(IGF)是一种普遍存在的多肽,参与人体生长发育的各个方面。此外,IGF被认为是具有有效抗凋亡活性的存活因子。干扰IGF的产生、分布或信号传导可能导致对凋亡刺激的更大易感性。在神经退行性疾病中,IGF似乎被前列腺素和促炎细胞因子拮抗。本文就特异性前列腺素、促炎因子、肿瘤坏死因子、白细胞介素-1、白细胞介素-6与IGF系统的关系作一综述。
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
自引率
0.00%
发文量
0
期刊最新文献
Introduction: low-saturated fat, high-carbohydrate diets: effects on triglyceride and LDL synthesis, the LDL receptor, and cardiovascular disease risk. Characterization of the calcium signaling system in the submandibular cell line SMG-C6. Role of nitric oxide and superoxide in acute cardiac allograft rejection in rats. Role of Sertoli cells in injury-associated testicular germ cell apoptosis. Cell death induction by CTL: perforin/granzyme B system dominantly acts for cell death induction in human hepatocellular carcinoma cells.
×
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