https://blog.superhyydl.org/tags/caf%E8%A1%B0%E8%80%81/Recent content in CAF衰老 on Superhyydl's BlogHugozh-cnSun, 06 Sep 2026 00:00:00 +0000https://blog.superhyydl.org/reading/macrophage-induced-senescent-cancer-associated-fibroblasts/Sun, 06 Sep 2026 00:00:00 +0000https://blog.superhyydl.org/reading/macrophage-induced-senescent-cancer-associated-fibroblasts/<h2 id="一句话亮点">一句话亮点</h2> <p>巨噬细胞来源的IL1B通过IL1R1诱导成纤维细胞衰老，衰老的成纤维细胞通过分泌IL6和CXCL12制造“耐药微环境”，削弱化疗效果。</p> <h2 id="背景痛点">背景/痛点</h2> <p>化疗是结直肠癌治疗的基石，但耐药问题始终是临床痛点。肿瘤微环境，特别是癌症相关成纤维细胞，已被广泛认为是肿瘤进展和耐药的“帮凶”。</p> <p>那么，CAF到底是怎么促进耐药的？作者注意到一个现象：CAF在肿瘤里会衰老。细胞衰老通常被看作是一种抑癌机制，但衰老的细胞会分泌大量的炎症因子、趋化因子和生长因子，这个现象叫衰老相关分泌表型（SASP）。SASP是一把双刃剑，它既能抑制肿瘤，也能在特定环境下促进肿瘤进展和耐药。</p> <p>所以问题就来了：肿瘤微环境里到底有没有衰老的CAF？如果有，它们是不是通过SASP在暗中推动化疗耐药？作者就是从这个假设出发，设计了一整条推理链。</p> <p><img alt="Fig. 1：Identifying sCAFs using a CSPM. A, Overview of the CSPM. B, Uniform Manifold Approximation and Projection for Dimension Reduction (UMAP) plot of the major cell types in the discovery cohort (CNP0004138). C, The senescence percentage of CAFs within each sample of the in-house cohort was calculated, and samples were classified as sCAF-high or sCAF-low according to the median value. D and E, Representative images and quantification of mIHC for sCAFs (p21+αSMA+ cells) in samples from the sCAF-high and sCAF-low groups. Data are mean ± SD. F, Heatmap displaying the AUCell scores of senescence gene sets across sCAFs and nsCAFs in the discovery cohort. G, Heatmap showing significant enrichment of senescence gene sets in sCAFs compared with nsCAFs across single-cell datasets, with color intensity reflecting the normalized enrichment score (NES) of GSEA. H, Dot plot comparing the expression of senescence markers across sCAFs and nsCAFs in" loading="lazy" src="https://blog.superhyydl.org/images/reading/macrophage-induced-senescent-cancer-associated-fibroblasts/figure-01.png"></p>