Inflammasome-associated pyroptosis and tumor angiogenesis in prostate cancer

Tumor angiogenesis in prostate cancer is increasingly recognized as a dynamic process shaped by inflammatory signaling, endothelial adaptation, and microenvironmental stress. However, the mechanistic contribution of inflammasome-associated pyroptosis to vascular remodeling remains insufficiently integrated, particularly in relation to functional vascular endpoints such as perfusion, permeability, and therapeutic delivery. This review critically evaluates current evidence linking inflammasome activation and pyroptotic signaling to angiogenic remodeling within prostate tumor microenvironments. Current mechanistic and translational studies addressing inflammasome signaling, gasdermin-associated membrane permeabilization, endothelial activation, cytokine amplification, and vascular remodeling were synthesized with emphasis on spatial heterogeneity, hypoxia-associated stress, and methodological limitations. Available evidence suggests that inflammasome-associated pathways may influence angiogenic remodeling through interleukin-1-mediated endothelial activation, myeloid-cell inflammatory amplification, extracellular signaling, and context-dependent pyroptotic responses. Emerging findings further indicate that vascular consequences vary according to metabolic stress, compartment-specific signaling, and local inflammatory states. However, interpretation remains limited by reliance on static tissue measurements, bulk inflammatory analyses, and indirect vascular readouts that insufficiently distinguish inflammasome priming from terminal pyroptotic execution. Inflammasome-associated pyroptotic signaling may contribute to vascular remodeling in prostate cancer under defined biological conditions, although substantial mechanistic and translational uncertainties remain. Improved integration of spatial inflammatory profiling and functional vascular assessment may support more precise therapeutic targeting and clinically relevant vascular interpretation in heterogeneous prostate tumor microenvironments.