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In an experimental rat model of immune-mediated glomerulonephritis, atorvastatin administration not only attenuated overall macrophage infiltration but also promoted a phenotypic reprogramming, evidenced by a diminution of M1-like macrophage subsets characterized by a pro-inflammatory cytokine/chemokine expression profile, alongside an expansion of M2 macrophage populations exhibiting anti-inflammatory, immunoregulatory, and tissue-reparative functional attributes, including IL-10–producing cells [255]

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