[过氧化物酶体增殖物激活受体-α在肾损伤中的作用:机制和治疗意义]。

Q3 Medicine
Jing Zhou, Li Luo, Junyu Zhu, Huaping Liang, Shengxiang Ao
{"title":"[过氧化物酶体增殖物激活受体-α在肾损伤中的作用:机制和治疗意义]。","authors":"Jing Zhou, Li Luo, Junyu Zhu, Huaping Liang, Shengxiang Ao","doi":"10.3760/cma.j.cn121430-20250318-00270","DOIUrl":null,"url":null,"abstract":"<p><p>Peroxisome proliferator activated receptor-α (PPAR-α) is significantly expressed in various tissues such as the liver, kidney, myocardium, and skeletal muscle, which plays a central role in the development of various diseases by regulating key physiological processes such as energy homeostasis, redox balance, inflammatory response, and ferroptosis. As an important metabolic and excretory organ of the body, renal dysfunction can lead to water and electrolyte imbalance, toxin accumulation, and multiple system complications. The causes of kidney injury are complex and diverse, including acute injury factors (such as ischemia/reperfusion, nephrotoxic drugs, septic shock, and immune glomerulopathy), as well as chronic progressive causes [such as metabolic disease-related nephropathy, hypertensive nephropathy (HN)], and risk factors such as alcohol abuse, obesity, and aging. This review briefly describes the structure, function, and activity regulation mechanism of PPAR-α, systematically elucidates the molecular regulatory network of PPAR-α in the pathological process of kidney injury including acute kidney injury (AKI) such as renal ischemia/reperfusion injury (IRI), drug-induced AKI, sepsis-associated acute kidney injury (SA-AKI), glomerulonephritis, chronic kidney disease (CKD) such as diabetic nephropathy (DN), HN, and other kidney injury, and summarizes the mechanisms related to PPAR-α regulation of kidney injury, including regulation of metabolism, antioxidation, anti-inflammation, anti-fibrosis, and anti-ferroptosis. This review also evaluates PPAR-α's medical value as a novel therapeutic target, and aims to provide theoretical basis for the development of kidney protection strategies based on PPAR-α targeted intervention.</p>","PeriodicalId":24079,"journal":{"name":"Zhonghua wei zhong bing ji jiu yi xue","volume":"37 7","pages":"693-697"},"PeriodicalIF":0.0000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Peroxisome proliferator activated receptor-α in renal injury: mechanisms and therapeutic implications].\",\"authors\":\"Jing Zhou, Li Luo, Junyu Zhu, Huaping Liang, Shengxiang Ao\",\"doi\":\"10.3760/cma.j.cn121430-20250318-00270\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Peroxisome proliferator activated receptor-α (PPAR-α) is significantly expressed in various tissues such as the liver, kidney, myocardium, and skeletal muscle, which plays a central role in the development of various diseases by regulating key physiological processes such as energy homeostasis, redox balance, inflammatory response, and ferroptosis. As an important metabolic and excretory organ of the body, renal dysfunction can lead to water and electrolyte imbalance, toxin accumulation, and multiple system complications. The causes of kidney injury are complex and diverse, including acute injury factors (such as ischemia/reperfusion, nephrotoxic drugs, septic shock, and immune glomerulopathy), as well as chronic progressive causes [such as metabolic disease-related nephropathy, hypertensive nephropathy (HN)], and risk factors such as alcohol abuse, obesity, and aging. This review briefly describes the structure, function, and activity regulation mechanism of PPAR-α, systematically elucidates the molecular regulatory network of PPAR-α in the pathological process of kidney injury including acute kidney injury (AKI) such as renal ischemia/reperfusion injury (IRI), drug-induced AKI, sepsis-associated acute kidney injury (SA-AKI), glomerulonephritis, chronic kidney disease (CKD) such as diabetic nephropathy (DN), HN, and other kidney injury, and summarizes the mechanisms related to PPAR-α regulation of kidney injury, including regulation of metabolism, antioxidation, anti-inflammation, anti-fibrosis, and anti-ferroptosis. This review also evaluates PPAR-α's medical value as a novel therapeutic target, and aims to provide theoretical basis for the development of kidney protection strategies based on PPAR-α targeted intervention.</p>\",\"PeriodicalId\":24079,\"journal\":{\"name\":\"Zhonghua wei zhong bing ji jiu yi xue\",\"volume\":\"37 7\",\"pages\":\"693-697\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Zhonghua wei zhong bing ji jiu yi xue\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3760/cma.j.cn121430-20250318-00270\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Zhonghua wei zhong bing ji jiu yi xue","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3760/cma.j.cn121430-20250318-00270","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0

摘要

过氧化物酶体增殖物激活受体-α (PPAR-α)在肝脏、肾脏、心肌和骨骼肌等多种组织中显著表达,通过调节能量稳态、氧化还原平衡、炎症反应和铁凋亡等关键生理过程,在多种疾病的发生发展中发挥核心作用。肾脏作为机体重要的代谢和排泄器官,肾功能不全可导致水电解质失衡、毒素积聚和多系统并发症。肾损伤的原因复杂多样,既有急性损伤因素(如缺血/再灌注、肾毒性药物、感染性休克、免疫性肾小球病变等),也有慢性进行性原因(如代谢性疾病相关性肾病、高血压肾病(HN)等),也有酗酒、肥胖、衰老等危险因素。本文简要介绍了PPAR-α的结构、功能和活性调控机制,系统阐述了PPAR-α在肾损伤病理过程中的分子调控网络,包括急性肾损伤(AKI)如肾缺血再灌注损伤(IRI)、药物性AKI、脓毒症相关性急性肾损伤(SA-AKI)、肾小球肾炎、慢性肾病(CKD)如糖尿病肾病(DN)、HN等肾损伤。总结了PPAR-α调控肾损伤的相关机制,包括调控代谢、抗氧化、抗炎症、抗纤维化、抗铁沉等。本文还对PPAR-α作为一种新的治疗靶点的医学价值进行了评价,旨在为开发基于PPAR-α靶向干预的肾保护策略提供理论依据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Peroxisome proliferator activated receptor-α in renal injury: mechanisms and therapeutic implications].

Peroxisome proliferator activated receptor-α (PPAR-α) is significantly expressed in various tissues such as the liver, kidney, myocardium, and skeletal muscle, which plays a central role in the development of various diseases by regulating key physiological processes such as energy homeostasis, redox balance, inflammatory response, and ferroptosis. As an important metabolic and excretory organ of the body, renal dysfunction can lead to water and electrolyte imbalance, toxin accumulation, and multiple system complications. The causes of kidney injury are complex and diverse, including acute injury factors (such as ischemia/reperfusion, nephrotoxic drugs, septic shock, and immune glomerulopathy), as well as chronic progressive causes [such as metabolic disease-related nephropathy, hypertensive nephropathy (HN)], and risk factors such as alcohol abuse, obesity, and aging. This review briefly describes the structure, function, and activity regulation mechanism of PPAR-α, systematically elucidates the molecular regulatory network of PPAR-α in the pathological process of kidney injury including acute kidney injury (AKI) such as renal ischemia/reperfusion injury (IRI), drug-induced AKI, sepsis-associated acute kidney injury (SA-AKI), glomerulonephritis, chronic kidney disease (CKD) such as diabetic nephropathy (DN), HN, and other kidney injury, and summarizes the mechanisms related to PPAR-α regulation of kidney injury, including regulation of metabolism, antioxidation, anti-inflammation, anti-fibrosis, and anti-ferroptosis. This review also evaluates PPAR-α's medical value as a novel therapeutic target, and aims to provide theoretical basis for the development of kidney protection strategies based on PPAR-α targeted intervention.

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
Zhonghua wei zhong bing ji jiu yi xue
Zhonghua wei zhong bing ji jiu yi xue Medicine-Critical Care and Intensive Care Medicine
CiteScore
1.00
自引率
0.00%
发文量
42
×
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:604180095
Book学术官方微信