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通过提高自噬和氧化还原平衡来激发策略,为多囊肾病的创新治疗开发提供新的思路。

Inspiring Tactics with the Improvement of Mitophagy and Redox Balance for the Development of Innovative Treatment against Polycystic Kidney Disease.

机构信息

Department of Food Science and Nutrition, Nara Women's University, Kita-Uoya Nishimachi, Nara 630-8506, Japan.

出版信息

Biomolecules. 2024 Feb 9;14(2):207. doi: 10.3390/biom14020207.

Abstract

Polycystic kidney disease (PKD) is the most common genetic form of chronic kidney disease (CKD), and it involves the development of multiple kidney cysts. Not enough medical breakthroughs have been made against PKD, a condition which features regional hypoxia and activation of the hypoxia-inducible factor (HIF) pathway. The following pathology of CKD can severely instigate kidney damage and/or renal failure. Significant evidence verifies an imperative role for mitophagy in normal kidney physiology and the pathology of CKD and/or PKD. Mitophagy serves as important component of mitochondrial quality control by removing impaired/dysfunctional mitochondria from the cell to warrant redox homeostasis and sustain cell viability. Interestingly, treatment with the peroxisome proliferator-activated receptor-α (PPAR-α) agonist could reduce the pathology of PDK and might improve the renal function of the disease via the modulation of mitophagy, as well as the condition of gut microbiome. Suitable modulation of mitophagy might be a favorable tactic for the prevention and/or treatment of kidney diseases such as PKD and CKD.

摘要

多囊肾病 (PKD) 是最常见的慢性肾脏病 (CKD) 的遗传形式,它涉及到多个肾脏囊肿的发展。针对 PKD 还没有足够的医学突破,PKD 的特征是局部缺氧和缺氧诱导因子 (HIF) 通路的激活。以下 CKD 的病理学可以严重引发肾脏损伤和/或肾衰竭。大量证据证实自噬在正常肾脏生理学和 CKD 和/或 PKD 的病理学中起着至关重要的作用。自噬作为线粒体质量控制的重要组成部分,通过从细胞中去除受损/功能失调的线粒体来保证氧化还原平衡并维持细胞活力。有趣的是,过氧化物酶体增殖物激活受体-α (PPAR-α) 激动剂的治疗可以减轻 PKD 的病理学,并通过调节自噬以及肠道微生物组来改善疾病的肾功能。适当调节自噬可能是预防和/或治疗 PKD 和 CKD 等肾脏疾病的有利策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7048/10886467/b15cdee71db7/biomolecules-14-00207-g001.jpg

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