Cellular signaling pathways involved in inflammation

Cellular signaling pathways involved in inflammation" refers to the complex network of molecular cascades activated within immune and non-immune cells that regulate the initiation, propagation, and resolution of inflammation. Key pathways include the nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK), Janus kinase-signal transducer and activator of transcription (JAK-STAT), and others. These pathways are activated by various receptors—such as Toll-like receptors (TLRs), cytokine receptors (e.g., TNF receptor, IL-1 receptor)—in response to infectious agents, cytokines, or cellular stress. They ultimately result in the modulation of gene expression, production of inflammatory mediators, immune cell activation, and changes in cellular survival, proliferation, and function. Dysregulation of these pathways contributes to diseases including chronic inflammatory disorders, autoimmune diseases, cancers, and age-related degenerative diseases. Because of their central role in disease, many components of these pathways are targets for therapeutic intervention[1][2][3][4][5][6][7][8]. Key point: This entry is not a single molecule or actionable target and should not be used as such in structured datasets of drug targets. If you wish to refer to a specific target involved in inflammatory signaling (such as "NF-κB subunit RelA"), a more specific entry should be selected.