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皮肤表现的线粒体功能障碍:文献复习。

Dermatologic Manifestations of Mitochondrial Dysfunction: A Review of the Literature.

机构信息

Morsani College of Medicine, University of South Florida, 560 Channelside Drive, Tampa, FL 33602, USA.

College of Osteopathic Medicine, Touro University, 1310 Club Dr, Vallejo, CA 94592, USA.

出版信息

Int J Mol Sci. 2024 Mar 14;25(6):3303. doi: 10.3390/ijms25063303.

Abstract

Mitochondria are eukaryotic cellular organelles that function in energy metabolism, ROS production, and programmed cell death. Cutaneous epithelial and hair follicle dermal papilla cells are energy-rich cells that thereby may be affected by mitochondrial dysfunction and DNA mutation accumulation. In this review, we aimed to summarize the medical literature assessing dermatologic conditions and outcomes associated with mitochondrial dysfunction. A search of PubMed and Embase was performed with subsequent handsearching to retrieve additional relevant articles. Mitochondrial DNA () deletions, mutation accumulation, and damage are associated with phenotypic signs of cutaneous aging, hair loss, and impaired wound healing. In addition, several dermatologic conditions are associated with aberrant mitochondrial activity, such as systemic lupus erythematosus, psoriasis, vitiligo, and atopic dermatitis. Mouse model studies have better established causality between mitochondrial damage and dermatologic outcomes, with some depicting reversibility upon restoration of mitochondrial function. Mitochondrial function mediates a variety of dermatologic conditions, and mitochondrial components may be a promising target for therapeutic strategies.

摘要

线粒体是真核细胞的细胞器,其功能在于能量代谢、ROS 生成和程序性细胞死亡。皮肤上皮和毛囊真皮乳头细胞是富含能量的细胞,因此可能受到线粒体功能障碍和 DNA 突变积累的影响。在这篇综述中,我们旨在总结评估与线粒体功能障碍相关的皮肤科状况和结果的医学文献。我们对 PubMed 和 Embase 进行了检索,并随后进行了手工检索以获取其他相关文章。线粒体 DNA(mtDNA)缺失、突变积累和损伤与皮肤衰老、脱发和伤口愈合受损的表型标志有关。此外,一些皮肤科疾病与异常的线粒体活性有关,如系统性红斑狼疮、银屑病、白癜风和特应性皮炎。小鼠模型研究更好地确立了线粒体损伤与皮肤科结果之间的因果关系,其中一些研究表明在恢复线粒体功能后具有逆转性。线粒体功能介导多种皮肤科疾病,线粒体成分可能是治疗策略的有前途的靶点。

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引用本文的文献

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Front Immunol. 2022 Jul 25;13:929520. doi: 10.3389/fimmu.2022.929520. eCollection 2022.
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