Nature子刊：刘光慧团队等揭示细胞衰老介导肺结核后遗症的分子机制，并提出潜在干预靶点

Core Insights - The article discusses a significant research study published in Nature Microbiology, which reveals the mechanisms behind lung damage in patients with a history of Mycobacterium tuberculosis infection [2][7]. Group 1: Research Findings - The research team constructed the first high-precision cellular molecular network of lung tissue post-tuberculosis infection, identifying cellular senescence and inflammation as key pathological features of lung damage [2][6]. - A total of 19 post-tuberculosis lung tissue samples and 13 matched normal lung samples were analyzed using single-cell transcriptomics, focusing on the lesions and surrounding areas [5]. - The study identified molecular characteristics associated with tuberculosis, including gene expression patterns related to senescence, inflammation, fibrosis, and apoptosis [6]. Group 2: Mechanisms and Implications - The research highlighted that exacerbated vascular inflammation is a critical feature of lung tissue following tuberculosis [6]. - The team discovered that silencing FOXO3 and treating with thrombin exacerbated endothelial cell senescence and inflammation, confirming the role of FOXO3 signaling and NF-κB-dependent thrombo-inflammatory processes [6]. - These findings provide new insights into the mechanisms of tuberculosis-related lung damage and suggest potential therapeutic targets to alleviate lung injury in affected patients [7].