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. Author manuscript; available in PMC: 2020 Mar 11.
Published in final edited form as: Nature. 2019 Sep 11;573(7774):430–433. doi: 10.1038/s41586-019-1546-z

Fig. 2.

Fig. 2.

Human cardiac fibroblast targets in disease. (a) Heat map of cardiac fibroblast gene expression changes (fold change) in patients with hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) when compared with non-failing hearts (NF). (n = 122 (NF), 27 (HCM), 89 (DCM)) Differential gene expression was performed using a linear model. (b) Immunohistochemistry for FAP (green) and cardiac Troponin (cardiomyocytes, red) expression in left ventricular free-wall sections from 6 individual human samples of NF (#1,2), HCM (#3,4), and DCM (#5,6). Representative images of 2 independent experiments with similar results. (c) Masson’s trichrome stain for fibrosis (blue; left, center) and immunohistochemistry for Fap (green; right) in adjacent WT mouse coronal heart sections 1 week after continuous saline (top) or angiotensin II/phenylephrine (bottom) treatment. Representative images of 2 independent experiments with similar results (n=7 biologically independent animals) (inset; left ventricle). Scale bars = 100μm.