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Following myocardial infarction(MI),macrophages infiltrate into the ischemic area to remove necrotic myocytes and stimulate fibroblasts to produce extracellular matrix(ECM)for the infarct scar.Post-MI,MMP-28-/-(null)mice demonstrate insufficient inflammation and ECM synthesis,indicating defects in macrophage and fibroblast physiology,which could occur through direct and indirect mechanisms.