ArticleMolecular biology reports2026
Impact of clarithromycin on monocytes-macrophages in patients with coronary arterial disease: a crucial study in cardiovascular research.
Article in Molecular biology reports, 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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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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5 authors.
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Abstract
backgroundBesides the known risk factor for coronary artery disease, macrolide antibiotics use has been associated with increased cardiovascular events. This risk is not fully understood, possibly due to macrolide antibiotic effects on macrophage subsets. This study evaluates clarithromycin on macrophage differentiation and polarization in healthy subjects and coronary artery disease patients. METHODS AND
resultsDifferentiation was induced with GM-CSF or M-CSF with/without clarithromycin. CD14, CD68 and CD163 expression were analyzed. Polarization to M1 or M2 macrophages was induced by IFN-γ and IL-4. In differentiation, clarithromycin decreased CD14 expression in M1 macrophages and reduced M2 markers (CD14. CD163) in healthy controls, but not in coronary artery disease patients. Clarithromycin also induced macrophage apoptosis in healthy subjects.
conclusionsClarithromycin appears to differentially modulate macrophage phenotype markers depending on the clinical context. In healthy subjects, it was associated with increased apoptosis in both M1 and M2 macrophages, reduced expression of CD14 and other M1-associated markers, and expression of the CD68 + subset. Additionally, M2-associated markers (CD206 and CD163) were reduced in both healthy subjects and CAD patients. The observed modulation of macrophage markers suggests that clarithromycin influences macrophage polarization pathways. In CAD patients, clarithromycin was associated with decreased expression of M1 markers (CD68 and CD14) and co-stimulatory molecules, consistent with previously described immunomodulatory effects.
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