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Abstract：
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.
摘要：
缺乏TOM5，一种线粒体蛋白，导致小鼠组织性肺炎（OP）。TOM5在OP发病中的临床意义和作用机制尚不清楚。我们证明，TOM5在OP患者的肺组织中显著增加，与胶原沉积呈正相关。在博来霉素诱导的慢性OP小鼠模型中，TOM5升高与肺纤维化一致。体外，TOM5调控肺泡上皮细胞线粒体膜电位。TOM5降低了早期凋亡细胞的比例，促进了细胞增殖。我们的研究揭示了TOM5在OP中的作用。
