
S100a4+ 肺泡巨噬細胞亞群通過促進脂肪酸代謝和血管生成，加速了癌前非典型腺瘤樣增生 (AAH) 的進展。


coremsg

Lung cancer is preceded by premalignant lesions, and what factors drive this transformation and the potential regulatory mode in the context of tumor initiation remain to be elucidated. In the course of precancerous lesions, we found a phasic shift in metabolic patterns. Macrophages are a heterogeneous cell population with high plasticity in the tumor microenvironment. Single-cell interaction and metabolic analyses highlighted a cellular state, S100a4+ alveolar macrophages, which exhibited distinct fatty acid metabolic activity, such as palmitic acid metabolism, at the atypical adenomatous hyperplasia stage, accompanied by an angiogenic promoting function in a pre-neoplastic setting. These findings were reproducible in human single-cell transcriptome and had been confirmed by histopathological staining and in vitro cell coculture assays. Taken together, the results from this study demonstrated that specific alveolar macrophage subset contributes to tumorigenesis by altering its metabolic state, suggesting that metabolic interventions targeting this cell state in the early stage of disease may delay neoplastic transformation of the lung epithelium.

### Competing Interest Statement

The authors have declared no competing interest.

S100a4+ alveolar macrophages accelerate the progression of precancerous atypical adenomatous hyperplasia by promoting fatty acid metabolism

s100a4-肺泡巨噬細胞通過促進脂肪酸代謝加速癌前非典型腺瘤樣增生的進展


S100a4+ 肺泡巨噬細胞通過促進脂肪酸代謝加速癌前非典型腺瘤樣增生的進展
