通过代谢晶状体的急性肾损伤:病理重编程机制和临床翻译潜力。

IF 3.2 3区 医学 Q2 PHYSIOLOGY
Frontiers in Physiology Pub Date : 2025-06-06 eCollection Date: 2025-01-01 DOI:10.3389/fphys.2025.1602865
Jingli Gao, Liuyifei Huang, Yuzhan Zhang, Lei Wei, Zhixiang Yu, Yan Xing, Jinguo Yuan, Xiaoxuan Ning, Shiren Sun
{"title":"通过代谢晶状体的急性肾损伤:病理重编程机制和临床翻译潜力。","authors":"Jingli Gao, Liuyifei Huang, Yuzhan Zhang, Lei Wei, Zhixiang Yu, Yan Xing, Jinguo Yuan, Xiaoxuan Ning, Shiren Sun","doi":"10.3389/fphys.2025.1602865","DOIUrl":null,"url":null,"abstract":"<p><p>Acute kidney injury (AKI) represents a clinical syndrome with a bleak short-term prognosis, posing a high risk for the development of chronic kidney diseases and end-stage kidney disease. The underlying mechanisms of AKI are still not fully understood, and effective intervention strategies remain elusive. Enormous energy is required to meet the functional activity in hypermetabolic tubular epithelial cells (TECs), the most vulnerable cell types during AKI. Recent evidence has shed light on the reprogramming of metabolic pathways and the shift in energy substrates under pathological conditions. The reprogrammed metabolic pathway initially serves to compensate for energy shortages and supply substrates for cell repair during the early stages of AKI. However, sustained metabolic dysregulation tend to become detrimental for tubular repair and regeneration. Intriguingly, dynamic alterations in specific metabolites extend beyond their conventional roles as metabolic byproducts, actively participating in pathophysiology through multifaceted regulatory mechanisms during AKI. As yet, clinical therapy for AKI has not yet incorporated the intervention of metabolic disorders, highlighting a vast potential for extensive application. This review aims to summarize recent studies on the role of metabolic pathway reprogramming and metabolites in AKI, while discussing promising therapeutic strategies targeting metabolic reprogramming.</p>","PeriodicalId":12477,"journal":{"name":"Frontiers in Physiology","volume":"16 ","pages":"1602865"},"PeriodicalIF":3.2000,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178853/pdf/","citationCount":"0","resultStr":"{\"title\":\"Acute kidney injury through a metabolic lens: pathological reprogramming mechanisms and clinical translation potential.\",\"authors\":\"Jingli Gao, Liuyifei Huang, Yuzhan Zhang, Lei Wei, Zhixiang Yu, Yan Xing, Jinguo Yuan, Xiaoxuan Ning, Shiren Sun\",\"doi\":\"10.3389/fphys.2025.1602865\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Acute kidney injury (AKI) represents a clinical syndrome with a bleak short-term prognosis, posing a high risk for the development of chronic kidney diseases and end-stage kidney disease. The underlying mechanisms of AKI are still not fully understood, and effective intervention strategies remain elusive. Enormous energy is required to meet the functional activity in hypermetabolic tubular epithelial cells (TECs), the most vulnerable cell types during AKI. Recent evidence has shed light on the reprogramming of metabolic pathways and the shift in energy substrates under pathological conditions. The reprogrammed metabolic pathway initially serves to compensate for energy shortages and supply substrates for cell repair during the early stages of AKI. However, sustained metabolic dysregulation tend to become detrimental for tubular repair and regeneration. Intriguingly, dynamic alterations in specific metabolites extend beyond their conventional roles as metabolic byproducts, actively participating in pathophysiology through multifaceted regulatory mechanisms during AKI. As yet, clinical therapy for AKI has not yet incorporated the intervention of metabolic disorders, highlighting a vast potential for extensive application. This review aims to summarize recent studies on the role of metabolic pathway reprogramming and metabolites in AKI, while discussing promising therapeutic strategies targeting metabolic reprogramming.</p>\",\"PeriodicalId\":12477,\"journal\":{\"name\":\"Frontiers in Physiology\",\"volume\":\"16 \",\"pages\":\"1602865\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2025-06-06\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178853/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Frontiers in Physiology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3389/fphys.2025.1602865\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"PHYSIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in Physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3389/fphys.2025.1602865","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

急性肾损伤(AKI)是一种短期预后不佳的临床综合征,具有发展为慢性肾脏疾病和终末期肾脏疾病的高风险。AKI的潜在机制尚不完全清楚,有效的干预策略仍然难以捉摸。高代谢小管上皮细胞(TECs)是AKI中最脆弱的细胞类型,需要大量的能量来满足其功能活动。最近的证据揭示了在病理条件下代谢途径的重编程和能量底物的转移。在AKI的早期阶段,重编程代谢途径最初用于补偿能量短缺并为细胞修复提供底物。然而,持续的代谢失调往往不利于小管的修复和再生。有趣的是,特定代谢物的动态变化超出了它们作为代谢副产物的传统作用,在AKI期间通过多方面的调节机制积极参与病理生理。迄今为止,AKI的临床治疗尚未纳入代谢紊乱的干预,突出了广泛应用的巨大潜力。本文旨在总结代谢途径重编程和代谢物在AKI中的作用的最新研究,同时讨论针对代谢重编程的治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Acute kidney injury through a metabolic lens: pathological reprogramming mechanisms and clinical translation potential.

Acute kidney injury (AKI) represents a clinical syndrome with a bleak short-term prognosis, posing a high risk for the development of chronic kidney diseases and end-stage kidney disease. The underlying mechanisms of AKI are still not fully understood, and effective intervention strategies remain elusive. Enormous energy is required to meet the functional activity in hypermetabolic tubular epithelial cells (TECs), the most vulnerable cell types during AKI. Recent evidence has shed light on the reprogramming of metabolic pathways and the shift in energy substrates under pathological conditions. The reprogrammed metabolic pathway initially serves to compensate for energy shortages and supply substrates for cell repair during the early stages of AKI. However, sustained metabolic dysregulation tend to become detrimental for tubular repair and regeneration. Intriguingly, dynamic alterations in specific metabolites extend beyond their conventional roles as metabolic byproducts, actively participating in pathophysiology through multifaceted regulatory mechanisms during AKI. As yet, clinical therapy for AKI has not yet incorporated the intervention of metabolic disorders, highlighting a vast potential for extensive application. This review aims to summarize recent studies on the role of metabolic pathway reprogramming and metabolites in AKI, while discussing promising therapeutic strategies targeting metabolic reprogramming.

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
CiteScore
6.50
自引率
5.00%
发文量
2608
审稿时长
14 weeks
期刊介绍: Frontiers in Physiology is a leading journal in its field, publishing rigorously peer-reviewed research on the physiology of living systems, from the subcellular and molecular domains to the intact organism, and its interaction with the environment. Field Chief Editor George E. Billman at the Ohio State University Columbus is supported by an outstanding Editorial Board of international researchers. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide.
×
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