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慢性肾脏病中的线粒体与血管钙化:从过去吸取的经验教训以改善未来治疗

Mitochondria and vascular calcification in chronic kidney disease: Lessons learned from the past to improve future therapy.

作者信息

Pongsuwan Karn, Kusirisin Prit, Narongkiattikhun Phoom, Chattipakorn Siriporn C, Chattipakorn Nipon

机构信息

Division of Nephrology, Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.

出版信息

J Cell Physiol. 2022 Dec;237(12):4369-4396. doi: 10.1002/jcp.30891. Epub 2022 Oct 2.


DOI:10.1002/jcp.30891
PMID:36183389
Abstract

Chronic kidney disease-mineral and bone disorders (CKD-MBD) is a common complication of CKD Stages 3-5. Hyperphosphatemia is one of the major metabolic components of CKD-MBD, frequently resulting in vascular calcification (VC) in advanced-stage patients. Also, a long duration of renal replacement therapy can cause the worsening of VC, leading to increased cardiovascular morbidity and mortality. Vascular smooth muscle cells play an important role in the development of VC through osteochondrogenic transformation and the apoptotic process. It has been shown that mitochondrial dysfunction is involved with CKD progression, and excessive oxidative stress can aggravate osteoblastic transformation and VC. Currently, novel interventions targeting mitochondrial function and dynamics, in addition to mitochondrial antioxidants, have been studied with the aim of attenuating VC. This review aims to comprehensively summarize and discuss the experimental and clinical reports concerning mitochondrial studies, along with the purpose of interventions that can improve the outcomes of VC among CKD patients.

摘要

慢性肾脏病-矿物质和骨异常(CKD-MBD)是3-5期慢性肾脏病的常见并发症。高磷血症是CKD-MBD的主要代谢成分之一,在晚期患者中常导致血管钙化(VC)。此外,长期的肾脏替代治疗会导致VC恶化,从而增加心血管疾病的发病率和死亡率。血管平滑肌细胞通过成骨软骨转化和凋亡过程在VC的发展中起重要作用。研究表明,线粒体功能障碍与CKD进展有关,过度的氧化应激会加重成骨细胞转化和VC。目前,除了线粒体抗氧化剂外,针对线粒体功能和动力学的新型干预措施也已被研究,旨在减轻VC。本综述旨在全面总结和讨论有关线粒体研究的实验和临床报告,以及改善CKD患者VC结局的干预措施的目的。

相似文献

[1]
Mitochondria and vascular calcification in chronic kidney disease: Lessons learned from the past to improve future therapy.

J Cell Physiol. 2022-12

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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引用本文的文献

[1]
The Roles of Lactate and Lactylation in Diseases Related to Mitochondrial Dysfunction.

Int J Mol Sci. 2025-7-24

[2]
Understanding Vascular Calcification in Chronic Kidney Disease: Pathogenesis and Therapeutic Implications.

Int J Mol Sci. 2024-12-5

[3]
Establishment and evaluation of a nomogram prediction model for the risk of vascular calcification in stage 5 chronic kidney disease patients.

Sci Rep. 2024-1-10

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