The canonical Wnt/beta-catenin signaling pathway has been mainly recognized as an important regulator of cell proliferation and differentiation during embryonic development. However, recent studies on the control and resolution of the inflammatory response, triggered by activation of different Toll-like receptors (TLRs) during bacterial infections, have demonstrated that physical interaction between the transcription factor nuclear factor kappa B (NF-kB) and beta-catenin switches off the expression of pro-inflammatory cytokines. Although some excellent work has been published, a deeper insight is mandatory to fully understand the complexity of interactions among molecules activated by binding of Wnt glycoproteins to their frizzle receptors and binding of ligands such as DAMPs, bacterial PAMPs or its virulence factors, to TLRs. Detailed functional and structural investigations on this subject matter are crucial to design new pharmacological drugs that help to control the inflammatory response. This task shall not be easy because these new drugs must not interfere with other beneficial processes activated by the tissue to restore the homeostatic state.
In this Research Topic we welcome researchers to submit original and review articles that contribute to mechanistically clarify how the activation of canonical Wnt/beta-catenin signaling pathway enhances or inhibits the inflammatory response, initiated by TLR activation.
The canonical Wnt/beta-catenin signaling pathway has been mainly recognized as an important regulator of cell proliferation and differentiation during embryonic development. However, recent studies on the control and resolution of the inflammatory response, triggered by activation of different Toll-like receptors (TLRs) during bacterial infections, have demonstrated that physical interaction between the transcription factor nuclear factor kappa B (NF-kB) and beta-catenin switches off the expression of pro-inflammatory cytokines. Although some excellent work has been published, a deeper insight is mandatory to fully understand the complexity of interactions among molecules activated by binding of Wnt glycoproteins to their frizzle receptors and binding of ligands such as DAMPs, bacterial PAMPs or its virulence factors, to TLRs. Detailed functional and structural investigations on this subject matter are crucial to design new pharmacological drugs that help to control the inflammatory response. This task shall not be easy because these new drugs must not interfere with other beneficial processes activated by the tissue to restore the homeostatic state.
In this Research Topic we welcome researchers to submit original and review articles that contribute to mechanistically clarify how the activation of canonical Wnt/beta-catenin signaling pathway enhances or inhibits the inflammatory response, initiated by TLR activation.
