Fatty acid‑binding proteins at the inflammation‑cancer interface: Isoform‑specific metabolic‑immune mechanisms and therapeutic implications (Review)

Fatty acid-binding proteins (FABPs) comprise ten mammalian isoforms (FABP1-FABP9 and FABP12), each a small intracellular lipid chaperone traditionally viewed as a mediator of fatty acid uptake, trafficking and metabolic partitioning.Evidence from metabolic disease, immunology and oncology indicates that selected FABP isoforms also regulate inflammatory signaling, immune-cell metabolism and tumor-stromal crosstalk.Prior reviews have mainly emphasized single isoforms of FABPs or single disease categories.The present narrative review organized FABP biology as a context-specific evidence map across the inflammation-cancer interface, in which each principal claim is reported together with the experimental system, with the outcome and limits of extrapolation described.The main mechanistic focus was FABP4, FABP5 and FABP7.The structural determinants of isoform specificity, ligand routing to nuclear receptors and the non-classical secretion of FABP4 as a circulating adipokine were summarized.The evidence supports a model in which FABPs may contribute to, rather than fully explain, the progression from metabolic stress to chronic low-grade inflammation, premalignant remodeling and the establishment of the tumor microenvironment.In the present model, FABP4 links adipocytes, macrophages, endothelial cells and tumor cells through fatty acid shuttling and inflammasome/cytokine signaling; FABP5 connects retinoic acid and peroxisome proliferator-activated receptor β/δ signaling with tumor-cell growth and T helper/regulatory T-cell balance; and FABP7 regulates neural-lineage tumor plasticity through ligand-dependent retinoid X receptor α signaling.In addition, translational evidence was stratified into clinically observed biomarkers, preclinical therapeutic targets and conceptual future technologies.Particular attention was paid to biomarker confounding by obesity, diabetes, age and sex, and to the therapeutic paradox in which FABP5 inhibition may suppress T helper 17 cell-driven inflammation while enhancing regulatory T-cell-mediated immunosuppression in cancer.This synthesis provides a restrained conceptual framework for stage-, isoform-and cell-type-specific FABP research.