ArticleMediators of inflammation2026
Macrophage-Myocyte Cross Talk Induces M1 Polarization and Inflammatory Cytokine Production During Cancer Cachexia.
Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- Macrophage-Myocyte Cross Talk Induces M1 Polarization and Inflammatory Cytokine Production During Cancer Cachexia.Mediators of inflammation · 2026Article
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7 authors.
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Abstract
Cancer cachexia (CC) significantly reduces survival in patients with cancer, and intramuscular inflammation plays an important role in disease progression. Macrophages, as key mediators of the innate immune response, contribute to muscle inflammation by secreting pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α), in response to various stimuli. Despite their importance, the mechanisms of macrophage polarization within the cachectic skeletal muscle and the subsequent impacts on muscle inflammation remain poorly understood. In this study, we used a murine model of CC to explore the interaction between macrophages and myocytes during muscle inflammation. Our results demonstrate that cachectic myocytes recruit M1-polarized macrophages that amplify local inflammation via the secretion of IL-1β, IL-6, and TNF-α. These findings underscore the pivotal role of macrophage-derived cytokines in the pathogenesis of cancer-induced muscle inflammation and suggest that targeting macrophage-driven inflammatory pathways may be an effective therapeutic strategy for mitigating muscle wasting in CC.
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