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. 2022 Aug 18;13:971416. doi: 10.3389/fimmu.2022.971416

Figure 2.

Figure 2

Cell type-dependent Hippo-YAP pathway regulate the inflammation response after Myocardial infarction. Cardiomyocyte-specific YAP inhibits inflammatory cells infiltration, including macrophages and neutrophils, and pro-inflammatory cytokines production through interacting with TLRs (toll-like receptors), thus improve cardiac function. Epicardial-specific YAP increases Tregs (T-regulatory cells) recruitment to inhibit macrophage infiltration and pro-inflammatory cytokines production through affecting IFN-γ (interferon γ) expression. Macrophage-specific knockdown of YAP decreases the accumulation of pro-inflammatory macrophages and enhances the accumulation of anti-inflammatory macrophages through regulating the expression of Spp1 (secreted phosphoprotein 1), IL6 (interleukin 6), ARG1 (arginase 1), CD163 to improve cardiac function. Cardiac fibroblast-specific knockdown of YAP inhibits fibroinflammatory response to decrease the recruitment of inflammatory cells, the production of pro-inflammatory cytokines and improve heart function. CSF1, colony stimulating factor 1; CXCL1, C-X-C Motif Chemokine Ligand 1; CXCL12, C-X-C Motif Chemokine Ligand 12; PRRs, pattern recognition receptors.