TOM5调节组织性肺炎中肺泡上皮细胞的线粒体膜电位。

IF 5.2 2区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Redox Report Pub Date : 2024-12-01 Epub Date: 2024-05-24 DOI:10.1080/13510002.2024.2354625

Yan Qian, Xiao Li, Xinyu Li, Xijie Zhang, Qi Yuan, Zhengxia Wang, Minghun Zhang, Mao Huang, Ningfei Ji

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引用次数: 0

摘要

线粒体蛋白 TOM5 缺乏会导致小鼠发生组织性肺炎（OP）。TOM5在OP发病机制中的临床意义和机制仍未确定。我们证实，TOM5 在 OP 患者的肺组织中明显增加，且与胶原沉积呈正相关。在博莱霉素诱导的小鼠慢性 OP 模型中，TOM5 的增加与肺纤维化一致。在体外，TOM5 可调节肺泡上皮细胞的线粒体膜电位。TOM5 可降低早期凋亡细胞的比例，促进细胞增殖。我们的研究揭示了TOM5在OP中的作用。

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TOM5 regulates the mitochondrial membrane potential of alveolar epithelial cells in organizing pneumonia.

Deficiency of TOM5, a mitochondrial protein, causes organizing pneumonia (OP) in mice. The clinical significance and mechanisms of TOM5 in the pathogenesis of OP remain elusive. We demonstrated that TOM5 was significantly increased in the lung tissues of OP patients, which was positively correlated with the collagen deposition. In a bleomycin-induced murine model of chronic OP, increased TOM5 was in line with lung fibrosis. In vitro, TOM5 regulated the mitochondrial membrane potential in alveolar epithelial cells. TOM5 reduced the proportion of early apoptotic cells and promoted cell proliferation. Our study shed light on the roles of TOM5 in OP.

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来源期刊

Redox Report 生物-生化与分子生物学

CiteScore

6.10

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Redox Report is a multidisciplinary peer-reviewed open access journal focusing on the role of free radicals, oxidative stress, activated oxygen, perioxidative and redox processes, primarily in the human environment and human pathology. Relevant papers on the animal and plant environment, biology and pathology will also be included. While emphasis is placed upon methodological and intellectual advances underpinned by new data, the journal offers scope for review, hypotheses, critiques and other forms of discussion.