FABPs bind fatty acids and other molecules (e.g., bile acids) and usher them to different intracellular and extracellular compartments. They also occur extracellularly, for example in the blood. The lipid chaperones FABPs reside and function in various cellular compartments: cytosol, nucleus, mitochondria, endoplasmic reticulum, lipid droplets, and endocytosis and exocytosis vesicles. We highlight the opportunities for improving diagnosis and treatment that open by encompassing all these pathological conditions within of a coherent nosological group, focusing on abnormal lipid chaperones as biomarkers of disease and etiological-pathogenic factors. In this review, we discuss the role of FABPs in the pathogenesis of metabolic syndrome, cancer, and neurological diseases. This entity is similar but separate from that encompassing the chaperonopathies pertaining to protein chaperones. We have assembled the disorders with abnormal FABPs as chaperonopathies in a distinct nosological entity. Deregulated expression and malfunction of FABPs can result from genetic alterations or posttranslational modifications and can be pathogenic. Increased circulating levels of FABPs are biomarkers of disorders such as obesity, insulin resistance, cardiovascular disease, and cancer. Quantitative and/or qualitative changes of FABPs are associated with pathological conditions. The various known FABP isoforms display distinctive tissue distribution, but some are active in more than one tissue. Fatty acid–binding proteins (FABPs) are lipid chaperones assisting in the trafficking of long-chain fatty acids with functions in various cell compartments, including oxidation, signaling, gene-transcription regulation, and storage.
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