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. 2020 Sep 4;21(18):6462. doi: 10.3390/ijms21186462

Figure 1.

Figure 1

Schematic representation of NF-κB and MAPK pathways. Chaperone proteins are released by cardiac cells and bind to surface receptors on cardiac cell types activating specific signaling chronic inflammation. Cell surface toll-like receptors (TLR) are activated by Pathogen-Associated Molecular Patterns (PAMPs) or Danger-Associated Molecular Patterns (DAMPs) to initiate intracellular signaling. Myeloid Differentiation Primary Response 88 (MYD88) binds to Interleukin-1 Receptor-Associated Kinase 4 (IRAK4) and IRAK1/2. The IRAK complex interacts with TNF Receptor Associated Factor 6 (TRAF6). TRAF6 forms a complex with Mitogen-Activated Protein Kinase Kinase Kinase 7 (MAP3K7 or TAK1), MAP3K7 Binding Protein 1 (TAB1) and 2 (TAB2). TAK1 then activates the IκB Kinase (IKK) complex, thus activating the Nuclear Factor Kappa B (NF-κB). The released NF-κB translocates into the nucleus and mediates the expression of a number of proinflammatory cytokine genes. In addition, TAK1 can activate the Mitogen-Activated Protein Kinase (MAPK) signaling pathway. The MAPK signaling pathway can activate the transcription factor Activator Protein 1 (AP-1). The activation of NF-κB and AP-1 contributes to the expression of proinflammatory cytokines, such as IL-1, IL-6 and TNF-α.