Fatty acid-binding protein 7 (FABP7) is a multifunctional lipid chaperone that is enriched in radial glia and astrocytes within the central nervous system (CNS) and is frequently upregulated in glioma. Beyond its established roles in glial development, lipid homeostasis, and circadian regulation, growing evidence positions FABP7 at the intersection of tumor metabolism, neuronal activity, and immune modulation in the brain. In this review, we integrate the physiological functions of FABP7 in glial cells with its tumor-intrinsic and microenvironmental roles in glioma. We summarize how gliomas co-opt FABP7-dependent metabolic, transcriptional, and post-transcriptional programs to promote stemness, lipid remodeling (e.g., altered fatty acid composition, lipid droplet formation, and lipid peroxidation resistance), inflammatory signaling, and invasive growth, including nuclear FABP7-mediated transcriptional activation linked to oncogene status. Furthermore, we discuss the role of FABP7 in shaping the tumor–neuro–immune interface, including regulating immunosuppressive gene networks, pro-tumoral macrophage polarization, resistance to T-cell-induced ferroptosis and immunotherapy, and tumor microtube-mediated integration into neuronal circuits to support glioma progression. Finally, we highlight therapeutic opportunities and challenges, including small-molecule FABP7 inhibitors, brain-directed delivery strategies, chronotherapeutic considerations, and combination approaches with immunotherapy. Collectively, this work positions FABP7-centered metabolic, circadian, and neuro-immune networks as potential vulnerabilities in glioma, linking fundamental glial biology to glioma therapeutics.

Circadian rhythms determine biological clocks that manage daily biological functions, including the sleep–wake rhythm, hormone release, and immune function. This can affect immune-mediated chronic inflammation in rheumatoid arthritis (RA), which leads to joint damage, pain, swelling, and morning stiffness. These clinical manifestations follow a distinct circadian rhythm because of the cyclic pattern of leukocyte movement, secretion of pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α at night, and fluctuations in cortisol and melatonin levels. Despite the increasing amount of evidence showing that insufficient sleep and disruption of the biological clock may play a role in RA development through suppression of the immune response in macrophages and resorption processes in osteoclasts, the cause of this phenomenon is still under investigation. The present-day guidelines continue to endorse DMARDs as the basis of treatment, while studies are exploring the role of chronotherapy as an adjunctive method for alleviating symptoms and enhancing disease outcomes. In this review, we explore current knowledge regarding the links between the molecular basis of circadian biology and the pathogenesis of RA, highlight recent trends in immune and bone remodeling mechanisms, and discuss modern possibilities for using chronotherapy, precision medicine, and advanced drug-delivery methods based on circadian rhythms to create optimal treatment strategies for RA.