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Fig. 7 Proposed model for the role of MyD88 in fibrosis and neutrophil recruitment following cardiac cryoinjury in zebrafish.a, TLRs (and IL-1Rs) recruit the adaptor molecule MyD88 upon ligand interaction. MyD88 in turn initiates signal transduction, which leads to the activation of several processes. In endocardial cells, PI3K/AKT pathway activation and fibrosis are controlled by the MyD88 signaling pathway. Neutrophil count is also partially affected by the levels of the endocardial chemokine Cxcl18b. Immune cells also activate a MyD88-mediated response leading to several processes, including the recruitment of more immune cells and the manifestation of an inflammatory response. b, In myd88?/? injured tissues, the MyD88 signaling pathway is not activated and thus, endocardial cells exhibit decreased activation of the PI3K/AKT pathway. myd88?/? injured tissues also exhibit decreased levels of the endocardial chemokine gene cxcl18b and an increase in features related to fibrosis. In addition, the neutrophil count appears significantly reduced. As the fibrotic and the immune responses are affected, other processes essential for successful regeneration are also impaired, including revascularization and CM proliferation.