Fig. 1

Cardiac FAP is upregulated and related to other activators of fibroblasts in HF. A Relative mRNA expression in control subjects (n = 10) and patients with HF (n = 26); and relative protein levels of FAP in control subjects (n = 8) and patients with AHF (n = 4) and chronic HF (n = 22) which are expressed in relative values with respect to the control group (FC). The control protein values have been set to 100. Immunohistochemistry of FAP (green) and DAPI (blue) expression in CNT and AHF patient. Arrows point to FAP-labeled activated fibroblasts. The yellow/orange spot is a lipofuscin particle. B Relative mRNA expression levels of genes with a profibrotic function in cardiac fibrosis in control subjects (n = 10) and patients with HF (n = 26). C–G Correlations between FAP mRNA levels and profibrotic gene mRNA levels. Bars represent mean ± SEM values. Figures reflect the relative expression (in arbitrary units) extracted from the mRNA-seq analysis for both patients and controls to provide an idea of the average expression of each of the molecules. A.u., arbitrary units. Correlations were determined using Spearman’s correlation coefficient. Control subjects (gray), HF patients (light blue), acute HF (mid blue), CHF (dark blue). *p < 0.05, **p < 0.01, ***p < 0.001. AEBP1 ae binding protein 1, AHF acute heart failure, CNT control, FAP fibroblast activation protein, HF heart failure, POSTN periostin, THBS4 thrombospondin 4, THY1 thy1 cell surface antigen; VIM vimentin