CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarization

Aims: Platelet activation plays a critical role in the pathogenesis of cardiovascular disease and inflammation, primarily through interactions with macrophages. CCL5, a chemokine stored in platelet α-granules, is released upon platelet activation. The present study determines the specific role of CCL5 in modulating platelet function, platelet-mediated macrophage polarization, and hypertensive cardiac remodelin. Conclusion: These findings underscore the detrimental role of CCL5-mediated platelet activation in triggering inflammatory responses and promoting M2 macrophage polarization during hypertensive cardiac remodeling, revealing the molecular mechanism by which CCL5 facilitates platelet-derived TGF-β1 signaling via NF-κB activation. These results elucidate the crosstalk between platelets and macrophages that exacerbates cardiac remodeling and highlight CCL5 as a potential therapeutic target for reducing inflammation and cardiac injury.