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Vitiligo auto-immune response upon oxidative stress-related mitochondrial DNA release opens up new therapeutic strategies.

作者信息

Sant'Anna-Silva Ana C B, Botton Thomas, Rossi Andrea, Dobner Jochen, Bzioueche Hanene, Thach Nguyen, Blot Lauriane, Pagnotta Sophie, Kleszczynski Konrad, Steinbrink Kerstin, Mazure Nathalie M, Rocchi Stéphane, Krutmann Jean, Passeron Thierry, Tulic Meri K

机构信息

Université Côte d'Azur, INSERM U1065, C3M, Nice, France.

IUF-Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany.

出版信息

Clin Transl Med. 2024 Aug;14(8):e1810. doi: 10.1002/ctm2.1810.

DOI:10.1002/ctm2.1810
PMID:39113238
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11306283/
Abstract
摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/1de1313cc7a0/CTM2-14-e1810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/7ef7ecccd602/CTM2-14-e1810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/bfb2552ee832/CTM2-14-e1810-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/dc7983d2d7a5/CTM2-14-e1810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/1de1313cc7a0/CTM2-14-e1810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/7ef7ecccd602/CTM2-14-e1810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/bfb2552ee832/CTM2-14-e1810-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/dc7983d2d7a5/CTM2-14-e1810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fbee/11306283/1de1313cc7a0/CTM2-14-e1810-g003.jpg

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引用本文的文献

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本文引用的文献

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Mitophagy and immune infiltration in vitiligo: evidence from bioinformatics analysis.自噬与免疫浸润在白癜风中的作用:生物信息学分析证据。
Front Immunol. 2023 May 23;14:1164124. doi: 10.3389/fimmu.2023.1164124. eCollection 2023.
2
Fumarate induces vesicular release of mtDNA to drive innate immunity.富马酸盐诱导线粒体 DNA 囊泡释放以驱动先天免疫。
Nature. 2023 Mar;615(7952):499-506. doi: 10.1038/s41586-023-05770-w. Epub 2023 Mar 8.
3
Analysis of Matched Skin and Gut Microbiome of Patients with Vitiligo Reveals Deep Skin Dysbiosis: Link with Mitochondrial and Immune Changes.
分析白癜风患者的匹配皮肤和肠道微生物组揭示了深度皮肤失调:与线粒体和免疫变化的关联。
J Invest Dermatol. 2021 Sep;141(9):2280-2290. doi: 10.1016/j.jid.2021.01.036. Epub 2021 Mar 24.
4
Loss of Function of the Gene Encoding the Histone Methyltransferase KMT2D Leads to Deregulation of Mitochondrial Respiration.编码组蛋白甲基转移酶 KMT2D 的基因功能丧失导致线粒体呼吸失调。
Cells. 2020 Jul 13;9(7):1685. doi: 10.3390/cells9071685.
5
Innate lymphocyte-induced CXCR3B-mediated melanocyte apoptosis is a potential initiator of T-cell autoreactivity in vitiligo.先天淋巴细胞诱导的 CXCR3B 介导的黑素细胞凋亡是白癜风中 T 细胞自身反应性的潜在启动子。
Nat Commun. 2019 May 16;10(1):2178. doi: 10.1038/s41467-019-09963-8.
6
Melatonin and its metabolites protect human melanocytes against UVB-induced damage: Involvement of NRF2-mediated pathways.褪黑素及其代谢产物可保护人类黑素细胞免受 UVB 诱导的损伤:涉及 NRF2 介导的途径。
Sci Rep. 2017 Apr 28;7(1):1274. doi: 10.1038/s41598-017-01305-2.
7
TLR3 and TLR4 But not TLR2 are Involved in Vogt-Koyanagi- Harada Disease by Triggering Proinflammatory Cytokines Production Through Promoting the Production of Mitochondrial Reactive Oxygen Species.Toll样受体3和Toll样受体4而非Toll样受体2通过促进线粒体活性氧的产生触发促炎细胞因子的产生而参与葡萄膜大脑炎。
Curr Mol Med. 2015;15(6):529-42. doi: 10.2174/1566524015666150731095611.
8
Human mitochondrial DNA: roles of inherited and somatic mutations.人类线粒体 DNA:遗传和体细胞突变的作用。
Nat Rev Genet. 2012 Dec;13(12):878-90. doi: 10.1038/nrg3275.
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Somatic mutations in the mitochondria of rheumatoid arthritis synoviocytes.类风湿性关节炎滑膜细胞线粒体中的体细胞突变。
Arthritis Res Ther. 2005;7(4):R844-51. doi: 10.1186/ar1752. Epub 2005 Apr 28.
10
Increased prevalence of vitiligo, but no evidence of premature ageing, in the skin of patients with bp 3243 mutation in mitochondrial DNA in the mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes syndrome (MELAS).线粒体脑肌病、乳酸酸中毒和卒中样发作综合征(MELAS)中,线粒体DNA存在bp 3243突变的患者皮肤中白癜风患病率增加,但无早衰迹象。
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