CCR2 dependent recruited pro-inflammatory monocytes contribute to the development of left ventricular hypertrophy in mice upon transverse aortic constriction.

In contrast to our investigations conducted in CX3CR1-deficient mice in which no hypertrophy could be detected, CCR2 ko mice exhibited a HW/BW-Index on day 3 that did not reach statistical significance when compared to control mice but increased to significant hypertrophy at day 6.

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Remarkably, we observed highly significant disparities in the fluorescence intensity of CD11b when comparing Ly6C high macrophages of Wt and CCR2-deficient mice across the different groups.

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