The M1/M2 polarization imbalance of tumor-associated macrophages represents the core immunological driver of colorectal cancer liver metastasis. M1 macrophages, induced by interferon-γ/lipopolysaccharide, highly express major histocompatibility complex class II molecules and produce reactive oxygen species to kill tumor cells; M2 macrophages are polarized by interleukin-4(IL-4)/IL-13 and dominate immune suppression and angiogenesis through IL-10, transforming growth factor-β, and vascular endothelial growth factor. In liver metastatic lesions, M2 macrophages predominate, promoting metastasis via pre-metastatic niche shaping and immune suppression. Non-coding RNAs, m6A modification, the succinate/HIF-1α axis, and the IDO1-kynurenine-AhR pathway regulate the polarization direction; the gut microbiota remotely influences polarization through the “gut-liver axis”. An “M2 polarization score” composed of exosomal CD163/CD206 combined with serum miR-146a-5p and miR-21-5p can predict the risk of liver metastasis. Therapeutic strategies such as CSF-1R inhibitors, CD40 agonists, and STAT3/PI3Kγ inhibitors reprogram macrophages, and their combination with immune checkpoint inhibitors significantly reduces liver metastatic burden. Current challenges focus on biomarker standardization and targeted therapeutic translation, necessitating multi-omics consensus subtyping to advance personalized immunotherapy.