Fig. 6.

MR deficiency in macrophages protects mice from cardiac inflammation, fibrosis, and heart dysfunction induced by aging. A Immunofluorescence micrographs of heart sections from old MR^flox and MR^LysMCre mice showing macrophages (CD68⁺ cells), fibroblasts (PDGFRα⁺ cells), and collagen type 1 immunoreactivity. B Sirius red/fast green staining of representative heart sections from old MR^flox and MR^LysMCre mice. C Interstitial fibrosis quantified by picrosirius red polarization microscopy, D cardiac IL-6 protein and E hydroxyproline levels in young and old MR^flox and MR^LysMCre mice. F Left ventricular maximal rate of pressure rise (dP/dt_max) and G maximal rate of pressure decline (dP/dt_min) measured in vivo with a conductance catheter in young and old MR^flox and MR^LysMCre mice. Aged MR^flox and MR^LysMCre mice were on average 22 (± 0.7) months old. Mean ± SEM, n = 3–9 per group; *p < 0.05