Senescent cancer-associated fibroblasts orchestrate early lymph node metastasis in pancreatic ductal adenocarcinoma through a sophisticated lactate-driven metabolic cascade. These aged fibroblasts increase glucose metabolism and lactate production, which activates lactylation-mediated serine metabolism that shields lymphatic endothelial cells from oxidative damage. Simultaneously, CCR4+ regulatory T cells accumulate around lymphatic vessels, creating an immunosuppressive environment that facilitates cancer spread. The histone deacetylase inhibitor chidamide selectively eliminated these senescent fibroblasts, reducing tumor progression and enhancing chemo-immunotherapy effectiveness. This discovery fundamentally reframes our understanding of how cellular aging contributes to cancer metastasis. Unlike previous focus on cancer cell mutations, this research reveals the tumor microenvironment's senescent components as active drivers of spread. The lactate-lactylation axis represents a novel therapeutic target, as lactylation has only recently been recognized as an epigenetic modification. The successful translation to clinical trials combining chidamide with standard therapy plus immune checkpoint inhibitors suggests senolytic approaches could transform pancreatic cancer treatment, historically one of the most lethal malignancies with five-year survival rates below 12%.