https://www.selleckchem.com/pr....oducts/2-6-dihydroxy
se in the DCM group (P0.001, respectively). These results suggest that activated PlGF/Flt-1 signalling and subsequent macrophage-mediated chronic non-infectious inflammation via MCP-1 in the myocardium are involved in the pathogenesis of UCM. These results suggest that activated PlGF/Flt-1 signalling and subsequent macrophage-mediated chronic non-infectious inflammation via MCP-1 in the myocardium are involved in the pathogenesis of UCM. The use of beta-blocker therapy in cardiac amyloidosis (CA) is debated. We aimed at
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