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Life sciences · Journal article
Frontiers in Microbiology · October 23, 2026
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Cancer-related fatigue (CRF) is a frequent and disabling symptom during cancer and anticancer therapy, and pathway-directed pharmacological treatment remains limited. This review examines CRF through the plant–microbiota–host axis, in which medicinal plant-derived bioactive compounds reshape gut microbial community structure and function and are in turn biotransformed by gut microbes into metabolites that host sensors detect. Tumor- and treatment-associated injury of the intestinal mucosa alters epithelial renewal, barrier selectivity, and microbial metabolism, reshaping host exposure to microbial products and metabolites. These changes generate molecular mediators, including short-chain fatty acids, tryptophan-derived metabolites, bile acids, and microbe-associated molecular patterns, which are detected by epithelial, immune, enteroendocrine, and neural sensors. We organize the evidence into mediator–sensor modules and discuss how vagal, humoral, and immune–metabolic routes may converge on brainstem and monoaminergic networks involved in activity, effort, and interoceptive malaise. Because direct causal evidence in CRF remains incomplete, we separate established biology from candidate mechanisms and define pharmacodynamic readouts that can test target engagement. Medicinal plant-derived compounds enter the framework upstream: their microbial conversion products engage the same mediator–sensor modules. We argue that future CRF studies should match the fatigue domain, biological subgroup, molecular target, and biomarker before efficacy is interpreted mechanistically; for plant-derived interventions, this matching must also include the administered compound and its microbially generated metabolites.