The Role of Mitochondrial Dysfunction in CKD-Related Vascular Calcification: From Mechanisms to Therapeutics

IF 8.3 2区材料科学 Q1 MATERIALS SCIENCE, MULTIDISCIPLINARY

ACS Applied Materials & Interfaces Pub Date : 2024-09-01 DOI:10.1016/j.ekir.2024.05.005

{"title":"The Role of Mitochondrial Dysfunction in CKD-Related Vascular Calcification: From Mechanisms to Therapeutics","authors":"","doi":"10.1016/j.ekir.2024.05.005","DOIUrl":null,"url":null,"abstract":"<div><p>Vascular calcification (VC) is a common complication of chronic kidney disease (CKD) and is closely associated with cardiovascular events. The transdifferentiation of vascular smooth muscles (VSMCs) into an osteogenic phenotype is hypothesized to be the primary cause underlying VC. However, there is currently no effective clinical treatment for VC. Growing evidence suggests that mitochondrial dysfunction accelerates the osteogenic differentiation of VSMCs and VC via multiple mechanisms. Therefore, elucidating the relationship between the osteogenic differentiation of VSMCs and mitochondrial dysfunction may assist in improving VC-related adverse clinical outcomes in patients with CKD. This review aimed to summarize the role of mitochondrial biogenesis, mitochondrial dynamics, mitophagy, and metabolic reprogramming, as well as mitochondria-associated oxidative stress (OS) and senescence in VC in patients with CKD to offer valuable insights into the clinical treatment of VC.</p></div>","PeriodicalId":5,"journal":{"name":"ACS Applied Materials & Interfaces","volume":null,"pages":null},"PeriodicalIF":8.3000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2468024924017121/pdfft?md5=7e3ef4f1533a7cc2a7f2c8beaae67446&pid=1-s2.0-S2468024924017121-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Materials & Interfaces","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2468024924017121","RegionNum":2,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MATERIALS SCIENCE, MULTIDISCIPLINARY","Score":null,"Total":0}

引用次数: 0

Abstract

Vascular calcification (VC) is a common complication of chronic kidney disease (CKD) and is closely associated with cardiovascular events. The transdifferentiation of vascular smooth muscles (VSMCs) into an osteogenic phenotype is hypothesized to be the primary cause underlying VC. However, there is currently no effective clinical treatment for VC. Growing evidence suggests that mitochondrial dysfunction accelerates the osteogenic differentiation of VSMCs and VC via multiple mechanisms. Therefore, elucidating the relationship between the osteogenic differentiation of VSMCs and mitochondrial dysfunction may assist in improving VC-related adverse clinical outcomes in patients with CKD. This review aimed to summarize the role of mitochondrial biogenesis, mitochondrial dynamics, mitophagy, and metabolic reprogramming, as well as mitochondria-associated oxidative stress (OS) and senescence in VC in patients with CKD to offer valuable insights into the clinical treatment of VC.

查看原文本刊更多论文

线粒体功能障碍在慢性肾脏病相关血管钙化中的作用：从机制到疗法

血管钙化（VC）是慢性肾脏病（CKD）的常见并发症，与心血管事件密切相关。据推测，血管平滑肌（VSMC）向成骨表型的转分化是导致血管钙化的主要原因。然而，目前尚无有效的临床治疗方法。越来越多的证据表明，线粒体功能障碍通过多种机制加速了 VSMCs 和 VC 的成骨分化。因此，阐明 VSMC 成骨分化与线粒体功能障碍之间的关系可能有助于改善 CKD 患者与 VC 相关的不良临床结局。本综述旨在总结线粒体生物生成、线粒体动力学、有丝分裂吞噬、代谢重编程以及线粒体相关氧化应激（OS）和衰老在 CKD 患者 VC 中的作用，从而为 VC 的临床治疗提供有价值的见解。

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分钟内获得全文求助全文

来源期刊

ACS Applied Materials & Interfaces 工程技术-材料科学：综合

CiteScore

16.00

自引率

6.30%

发文量

4978

审稿时长

1.8 months

期刊介绍： ACS Applied Materials & Interfaces is a leading interdisciplinary journal that brings together chemists, engineers, physicists, and biologists to explore the development and utilization of newly-discovered materials and interfacial processes for specific applications. Our journal has experienced remarkable growth since its establishment in 2009, both in terms of the number of articles published and the impact of the research showcased. We are proud to foster a truly global community, with the majority of published articles originating from outside the United States, reflecting the rapid growth of applied research worldwide.