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慢性肾脏病的线粒体病理生理学。

Mitochondrial Pathophysiology on Chronic Kidney Disease.

机构信息

Department of Anatomy, Unit for Multidisciplinary Research in Biomedicine (UMIB), Institute of Biomedical Sciences Abel Salazar (ICBAS), University of Porto, 4050-523 Porto, Portugal.

Department of Nephrology, Santo António General Hospital (Hospital Center of Porto, EPE), 4099-001 Porto, Portugal.

出版信息

Int J Mol Sci. 2022 Feb 4;23(3):1776. doi: 10.3390/ijms23031776.

DOI:10.3390/ijms23031776
PMID:35163697
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8836100/
Abstract

In healthy kidneys, interstitial fibroblasts are responsible for the maintenance of renal architecture. Progressive interstitial fibrosis is thought to be a common pathway for chronic kidney diseases (CKD). Diabetes is one of the boosters of CKD. There is no effective treatment to improve kidney function in CKD patients. The kidney is a highly demanding organ, rich in redox reactions occurring in mitochondria, making it particularly vulnerable to oxidative stress (OS). A dysregulation in OS leads to an impairment of the Electron transport chain (ETC). Gene deficiencies in the ETC are closely related to the development of kidney disease, providing evidence that mitochondria integrity is a key player in the early detection of CKD. The development of novel CKD therapies is needed since current methods of treatment are ineffective. Antioxidant targeted therapies and metabolic approaches revealed promising results to delay the progression of some markers associated with kidney disease. Herein, we discuss the role and possible origin of fibroblasts and the possible potentiators of CKD. We will focus on the important features of mitochondria in renal cell function and discuss their role in kidney disease progression. We also discuss the potential of antioxidants and pharmacologic agents to delay kidney disease progression.

摘要

在健康的肾脏中,间质成纤维细胞负责维持肾脏结构。进行性间质纤维化被认为是慢性肾脏病(CKD)的共同途径。糖尿病是 CKD 的助推因素之一。目前尚无有效的治疗方法可以改善 CKD 患者的肾功能。肾脏是一个高需求的器官,富含在线粒体中发生的氧化还原反应,使其特别容易受到氧化应激(OS)的影响。OS 的失调会导致电子传递链(ETC)的损伤。ETC 中的基因缺陷与肾脏疾病的发展密切相关,这为线粒体完整性是 CKD 早期检测的关键因素提供了证据。由于目前的治疗方法无效,因此需要开发新型 CKD 治疗方法。抗氧化靶向治疗和代谢方法显示出有希望的结果,可以延缓与肾脏疾病相关的一些标志物的进展。在此,我们讨论了成纤维细胞的作用和可能的起源以及 CKD 的可能促进因素。我们将重点讨论线粒体在肾细胞功能中的重要特征,并讨论它们在肾脏疾病进展中的作用。我们还讨论了抗氧化剂和药物制剂延缓肾脏疾病进展的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c6/8836100/4390568ba5ff/ijms-23-01776-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c6/8836100/b02cdda0f0cf/ijms-23-01776-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c6/8836100/b59555bf26d5/ijms-23-01776-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c6/8836100/4390568ba5ff/ijms-23-01776-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c6/8836100/b02cdda0f0cf/ijms-23-01776-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c6/8836100/b59555bf26d5/ijms-23-01776-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87c6/8836100/4390568ba5ff/ijms-23-01776-g003.jpg

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