CCR2 and Myocardial fibrosis: In the animal model of Ang II infusion or gene knockout, the pharmacologic blockade of the AT1R, specific ablation of macrophages, or abrogation of MCP-1 or CCR2+ markedly prevents the release of vascular inflammatory cytokines, attenuates the early development of myocardial fibrosis, and suppresses the progression of concentric to eccentric cardiac hypertrophy by reducing the numbers of non-resident CCR2+ macrophages [15,93,94,95].