One of the significant advances in the biology of idiopathic pulmonary fibrosis (IPF) has been the recognition of fibroblast heterogeneity in the lung. Fibroblast heterogeneity can be interpreted as fibroblast subtypes, probably derived from distinct mesenchymal lineages, as well as various activation states, such as proliferation, matrix production and invasiveness. With great interest, we read the original work by Mayr et al. [1] presenting a concept that the Sfrp1⁺ transitional fibroblasts with low invasive capacity emerge early after bleomycin-induced injury and ultimately transit to Spp1/Cthrc1⁺ matrix-producing (myo)fibroblasts with the driving force of transforming growth factor (TGF)β1 signalling from myeloid and epithelial lineages. This study largely aligns with our recent publication proposing that multiple fibroblast subtypes from IPF lungs contribute to the invasive phenotype of fibroblasts and the matrix deposition in pulmonary fibrosis [2].

特发性肺纤维化（IPF）生物学的重大进展之一是对肺部成纤维细胞异质性的认识。成纤维细胞异质性可以解释为成纤维细胞亚型，可能源自不同的间充质谱系，以及各种激活状态，例如增殖、基质产生和侵袭性。我们饶有兴趣地阅读了M的原著艾尔 等人。 [1]提出了这样的概念：具有低侵袭能力的Sfrp1 ⁺移行成纤维细胞在博来霉素诱导损伤后早期出现，并最终在转化生长因子（TGF）β1的驱动力下转变为Spp1/Cthrc1 ⁺基质生成（肌）成纤维细胞来自骨髓和上皮谱系的信号传导。这项研究与我们最近发表的文章基本一致，提出来自 IPF 肺部的多种成纤维细胞亚型有助于成纤维细胞的侵袭表型和肺纤维化中的基质沉积 [2]。