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. 2019 Nov 16;31:138–149. doi: 10.1016/j.molmet.2019.10.008

Figure 3.

Figure 3

Deletion of FPR2 in mice advances cardiac aging with disruption in the integrin signaling pathway. (A) Heat map representing changes in the extracellular matrix (ECM) gene expression profile in WT and FPR2−/− mice at 7 months of age. Color-coded bar graph representing the change in expression from green (−1 lowest decrease) to red (+1 highest increase). Bar graph representing significantly (B) downregulated and (C) upregulated ECM genes in FPR2−/− mice compared with WT at 7 months of age. (D) Functional classification of genes using panther pathway analysis showing FPR2 deletion affected the integrin signaling pathway. (E, F, G) Decreased mRNA expression of immune-responsive LOXs (ALOX-5, ALOX-12, ALOX-15) in the LV of FPR2−/− mice at 2 and 7 months of age compared with WT. (H, I) Increased mRNA expression of COX-1 and COX-2 in the LV of FPR2−/− mice at 2 and 7 months of age as compared with WT. n = 5 mice per group; *p < 0.05 vs corresponding age-matched controls.