ArticleAdvanced healthcare materials2026
Microfluidic Modeling of Macrophage-Induced Cardiac Inflammation Using NF-κB Reporter Cardiomyocytes.
Article in Advanced healthcare materials, 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
Inflammation is a key driver of cardiac disease progression, including heart failure and myocardial infarction, with macrophage-cardiomyocyte interactions playing a central role in shaping the local inflammatory microenvironment. Prolonged exposure to pro-inflammatory cytokines, many produced by macrophages, induces cardiomyocyte stress, dysfunction, and pathological tissue remodeling. However, the spatial and temporal dynamics of this crosstalk remain poorly understood, limiting the development of targeted therapies. To address this gap, we developed an in vitro cardiac inflammation model that enables controlled investigation of macrophage-cardiomyocyte interactions. Cardiomyocytes were transduced with an NF-κB-responsive fluorescent reporter to allow real-time monitoring of inflammatory signaling. MATLAB-based simulations were used to optimize medium delivery and cell densities by modeling TNFα diffusion. Using a multiplex microfluidic co-culture chip, we identified the TNFα threshold of 50 ng mL
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