ArticleJournal of inflammation research2026
Chronic Intermittent Hypoxia Promotes Macrophage Inflammation Through Reduction of Adipocyte‑Derived Adiponectin.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Macrophage-driven inflammation in adipose tissue contributes to chronic intermittent hypoxia (CIH)-induced metabolic disorders, but the underlying mechanisms remain unclear. Adiponectin (Ad), an abundant adipokine secreted by adipocytes, plays a crucial role in insulin sensitivity. We tested the hypothesis that CIH-induced macrophage inflammation requires adipocyte-derived paracrine signals and that Ad attenuates this process. Methods: Using a co-culture approach, we investigated the roles of adipocytes and Ad in CIH-induced macrophage inflammation. Direct co-culture involved physical interaction between iBMDM macrophages and 3T3-L1 adipocytes, while indirect co-culture used adipocyte-conditioned media. After CIH and Ad treatment, inflammatory factor levels in conditioned media were quantified. Statistical significance was set at P < 0.05. Results: CIH did not directly trigger inflammatory factor release from individually cultured iBMDM cells or 3T3-L1 adipocytes. However, CIH significantly increased inflammatory factor release in co-cultured cells. Ad alleviated the pro-inflammatory effect of adipocytes on macrophages under CIH conditions. Conclusion: CIH disrupts adipocyte function and promotes macrophage inflammation via paracrine mechanisms.
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