Targeting TLR4/MAPKs signaling pathway: A better option for therapeutic inhibition of atherosclerosis

Figure 1 Proposed mechanism of toll-like receptor 4/mitogen activated protein kinases signaling pathway and its suitable targets for therapeutic inhibition of atherosclerosis. The activation of toll-like receptor 4 (TLR4) receptor by various external stimulus leads to the transmittance of signal from cell surface to interior. The TLR4 in turn activates cascades of proteins and finally activates the IKK dependent phosphorylation of IκB and also there is an activation of mitogen activated protein kinase (MAPKs) which also contribute to the dissociation of IκB and the nuclear translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65 subunit, thereby activating key inflammatory cascade activation by MAPKs/NF-κB signaling pathway to induce toxicity by activating different inflammatory parameters. Hence we can target the TLR4/MAPKs signaling pathway at different places in the signaling pathway which indicated in the diagram. IKK: IκB kinase: JNK- c-Jun N-terminal kinases: ERK: Extracellular signal regulated kinases; MEKK1: Mitogen-activated protein kinase kinase kinase 1.