这份研究文章及其摘要讨论了巨胞饮作用在胰腺癌相关成纤维细胞（CAFs）亚型维持中的作用，尤其是在代谢压力（如谷氨酰胺缺乏）下。作者证明了抑制巨胞饮作用会促使肌成纤维细胞（myCAFs）转化为炎症性成纤维细胞（iCAFs），这是一个依赖于MEK-ERK信号通路的、代谢应激驱动的过程。这种CAF可塑性的改变重塑了胰腺肿瘤微环境，具体表现为胶原沉积减少、血管扩张以及T细胞浸润增加。研究结果表明，通过抑制巨胞饮作用来改变基质结构，可以增强胰腺导管腺癌（PDAC）对免疫疗法和化疗的敏感性，支持将这种抑制策略作为一种有前景的联合治疗方法。References: Zhang Y, Ling L, Murad R, et al. Macropinocytosis maintains CAF subtype identity under metabolic stress in pancreatic cancer[J]. Cancer Cell, 2025, 43(9): 1677-1696. e15.
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