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线粒体:对抗类风湿性关节炎的一项突破。

Mitochondria: a breakthrough in combating rheumatoid arthritis.

作者信息

Li Shuang, Huo Chenlu, Liu Anting, Zhu Yan

机构信息

Graduate School of Anhui University of Chinese Medicine, Hefei, Anhui, China.

Department of Geriatrics, The Second Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, China.

出版信息

Front Med (Lausanne). 2024 Aug 5;11:1439182. doi: 10.3389/fmed.2024.1439182. eCollection 2024.

DOI:10.3389/fmed.2024.1439182
PMID:39161412
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11330793/
Abstract

As a chronic autoimmune disease with complex aetiology, rheumatoid arthritis (RA) has been demonstrated to be associated with mitochondrial dysfunction since mitochondrial dysfunction can affect the survival, activation, and differentiation of immune and non-immune cells involved in the pathogenesis of RA. Nevertheless, the mechanism behind mitochondrial dysfunction in RA remains uncertain. Accordingly, this review addresses the possible role and mechanisms of mitochondrial dysfunction in RA and discusses the potential and challenges of mitochondria as a potential therapeutic strategy for RA, thereby providing a breakthrough point in the prevention and treatment of RA.

摘要

类风湿关节炎(RA)作为一种病因复杂的慢性自身免疫性疾病,已被证明与线粒体功能障碍有关,因为线粒体功能障碍会影响参与RA发病机制的免疫和非免疫细胞的存活、激活和分化。然而,RA中线粒体功能障碍背后的机制仍不明确。因此,本综述探讨了线粒体功能障碍在RA中的可能作用和机制,并讨论了线粒体作为RA潜在治疗策略的潜力和挑战,从而为RA的预防和治疗提供一个突破点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/d689ab22a6e1/fmed-11-1439182-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/b24b52ea495d/fmed-11-1439182-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/3307488f4a48/fmed-11-1439182-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/6422f3fa2c1b/fmed-11-1439182-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/d689ab22a6e1/fmed-11-1439182-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/b24b52ea495d/fmed-11-1439182-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/3307488f4a48/fmed-11-1439182-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/6422f3fa2c1b/fmed-11-1439182-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91a6/11330793/d689ab22a6e1/fmed-11-1439182-g004.jpg

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本文引用的文献

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Arthritis Res Ther. 2024 May 7;26(1):97. doi: 10.1186/s13075-024-03329-2.
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A systematic review on the biochemical threshold of mitochondrial genetic variants.线粒体遗传变异生化阈值的系统评价。
Genome Res. 2024 Apr 25;34(3):341-365. doi: 10.1101/gr.278200.123.
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Caspase-3 targets pro-interleukin-1β (IL-1β) to restrict inflammation.半胱天冬酶-3 靶向前白细胞介素-1β(IL-1β)以限制炎症。
慢性低水平干扰素-γ表达破坏肾巨噬细胞中的线粒体复合物I活性:狼疮性肾炎发病机制的早期机制驱动因素。
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FEBS Lett. 2024 Jun;598(11):1366-1374. doi: 10.1002/1873-3468.14864. Epub 2024 Mar 30.
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Exosomes derived from diabetic serum accelerate the progression of osteoarthritis.源自糖尿病血清的外泌体加速骨关节炎的进展。
Arch Biochem Biophys. 2024 May;755:109960. doi: 10.1016/j.abb.2024.109960. Epub 2024 Mar 19.
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