Fig. 1

Heterogeneity of TAMs in tumor microenvironment witnessed in the era of single-cell omics. a,b Single-cell multi-omics underscore TAMs' diverse origins, phenotypes, and functions shaped by the tumor microenvironment, highlighting metabolic reprogramming's influence on TAM heterogeneity. c,d Beyond the traditional polarization dichotomy, Ruo-Yu Ma et al. classified seven TAM subtypes characterized by specific gene signatures and functions using single-cell omics, named: interferon-stimulated (IFN-TAMs), immune-modulated (Reg-TAMs), inflammatory cytokine-enriched (Inflam-TAMs), lipid-associated (LA-TAMs), pro-angiogenic (Angio-TAMs), RTM-like (RTM-TAMs), and proliferative TAMs (Prolif-TAMs). e TAMs' heterogeneity is linked to their varied functions, with emerging research clarifying their roles in tumor progression. MDP Myeloid differentiation primary response protein, RTM Resident tissue macrophages, EMP Erythromyeloid progenitors, Treg Regulatory T cells, MDSC Myeloid-derived suppressor cells, Teff Effector T cells, NK Natural killer cells, ECM Extracellular matrix, CAF Cancer-associated fibroblasts, HGF Hepatocyte growth factor, CCL18 Chemokine (C–C motif) ligand 18, EGF Epidermal growth factor, MMP Matrix metalloproteinase, CXCR4 C-X-C chemokine receptor type 4, SPP1 Secreted phosphoprotein 1, VEGFR Vascular endothelial growth factor receptor, MARCO Macrophage receptor with collagenous structure, Arg1 Arginase 1, iNOS Inducible nitric oxide synthase, IDO Indoleamine 2,3-dioxygenase