PPARδ,心脏病的潜在治疗靶点。

Nuclear Receptor Research Pub Date : 2018-01-01 Epub Date: 2018-10-30 DOI:10.32527/2018/101375
Qinglin Yang, Qinqiang Long
{"title":"PPARδ,心脏病的潜在治疗靶点。","authors":"Qinglin Yang, Qinqiang Long","doi":"10.32527/2018/101375","DOIUrl":null,"url":null,"abstract":"<p><p>The nuclear receptor peroxisome proliferator-activated receptor <i>δ</i> (PPAR<i>δ</i>) can transcriptionally regulate target genes. PPAR<i>δ</i> exerts essential regulatory functions in the heart, which requires constant energy supply. PPAR<i>δ</i> plays a key role in energy metabolism, controlling not only fatty acid (FA) and glucose oxidation, but also redox homeostasis, mitochondrial biogenesis, inflammation, and cardiomyocyte proliferation. PPAR<i>δ</i> signaling is impaired in the heart under various pathological conditions, such as pathological cardiac hypertrophy, myocardial ischemia/reperfusion, doxorubicin cardiotoxicity and diabetic cardiomyopathy. PPAR<i>δ</i> deficiency in the heart leads to cardiac dysfunction, myocardial lipid accumulation, cardiac hypertrophy/remodeling and heart failure. This article provides an up-today overview of this research area and discusses the role of PPAR<i>δ</i> in the heart in light of the complex mechanisms of its transcriptional regulation and its potential as a translatable therapeutic target for the treatment of cardiac disorders.</p>","PeriodicalId":30720,"journal":{"name":"Nuclear Receptor Research","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6481951/pdf/","citationCount":"0","resultStr":"{\"title\":\"PPAR<i>δ</i>, a Potential Therapeutic Target for Heart Disease.\",\"authors\":\"Qinglin Yang, Qinqiang Long\",\"doi\":\"10.32527/2018/101375\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The nuclear receptor peroxisome proliferator-activated receptor <i>δ</i> (PPAR<i>δ</i>) can transcriptionally regulate target genes. PPAR<i>δ</i> exerts essential regulatory functions in the heart, which requires constant energy supply. PPAR<i>δ</i> plays a key role in energy metabolism, controlling not only fatty acid (FA) and glucose oxidation, but also redox homeostasis, mitochondrial biogenesis, inflammation, and cardiomyocyte proliferation. PPAR<i>δ</i> signaling is impaired in the heart under various pathological conditions, such as pathological cardiac hypertrophy, myocardial ischemia/reperfusion, doxorubicin cardiotoxicity and diabetic cardiomyopathy. PPAR<i>δ</i> deficiency in the heart leads to cardiac dysfunction, myocardial lipid accumulation, cardiac hypertrophy/remodeling and heart failure. This article provides an up-today overview of this research area and discusses the role of PPAR<i>δ</i> in the heart in light of the complex mechanisms of its transcriptional regulation and its potential as a translatable therapeutic target for the treatment of cardiac disorders.</p>\",\"PeriodicalId\":30720,\"journal\":{\"name\":\"Nuclear Receptor Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6481951/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nuclear Receptor Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.32527/2018/101375\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2018/10/30 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nuclear Receptor Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.32527/2018/101375","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2018/10/30 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

核受体过氧化物酶体增殖激活受体δ(PPARδ)可以转录调节靶基因。PPARδ 在需要持续能量供应的心脏中发挥着重要的调节功能。PPARδ 在能量代谢中发挥关键作用,不仅控制脂肪酸(FA)和葡萄糖氧化,还控制氧化还原平衡、线粒体生物生成、炎症和心肌细胞增殖。在各种病理情况下,如病理性心肌肥厚、心肌缺血/再灌注、多柔比星心脏毒性和糖尿病心肌病等,心脏中的 PPARδ 信号都会受损。心脏中 PPARδ 的缺乏会导致心脏功能障碍、心肌脂质堆积、心脏肥大/重塑和心力衰竭。本文概述了这一研究领域的最新进展,并根据 PPARδ 转录调控的复杂机制及其作为治疗心脏疾病的可转化治疗靶点的潜力,讨论了 PPARδ 在心脏中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

PPAR<i>δ</i>, a Potential Therapeutic Target for Heart Disease.

PPAR<i>δ</i>, a Potential Therapeutic Target for Heart Disease.

PPAR<i>δ</i>, a Potential Therapeutic Target for Heart Disease.

PPARδ, a Potential Therapeutic Target for Heart Disease.

The nuclear receptor peroxisome proliferator-activated receptor δ (PPARδ) can transcriptionally regulate target genes. PPARδ exerts essential regulatory functions in the heart, which requires constant energy supply. PPARδ plays a key role in energy metabolism, controlling not only fatty acid (FA) and glucose oxidation, but also redox homeostasis, mitochondrial biogenesis, inflammation, and cardiomyocyte proliferation. PPARδ signaling is impaired in the heart under various pathological conditions, such as pathological cardiac hypertrophy, myocardial ischemia/reperfusion, doxorubicin cardiotoxicity and diabetic cardiomyopathy. PPARδ deficiency in the heart leads to cardiac dysfunction, myocardial lipid accumulation, cardiac hypertrophy/remodeling and heart failure. This article provides an up-today overview of this research area and discusses the role of PPARδ in the heart in light of the complex mechanisms of its transcriptional regulation and its potential as a translatable therapeutic target for the treatment of cardiac disorders.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
审稿时长
12 weeks
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信