Pro-inflammatory signaling pathways

Pro-inflammatory signaling pathways refer to the molecular communication networks activated by cellular receptors in response to infectious or non-infectious inflammatory stimuli. Pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) trigger pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), NOD-like receptors (NLRs), and C-type lectin receptors, initiating downstream signaling through NF-κB, MAPK, and JAK-STAT pathways. These cascades result in the transcription of genes encoding pro-inflammatory cytokines, chemokines, and other mediators that coordinate immune cell recruitment, activation, and the resolution or propagation of inflammation. Dysregulation or chronic activation of these pathways is linked to a wide range of diseases including autoimmune disorders, infection, cancer, and cardiovascular and neurodegenerative diseases. In summary, "Pro-inflammatory signaling pathways" describe an important biological process, not an individual target molecule or receptor; thus, it cannot be mapped to a canonical target entity for drug discovery or biomarker purposes, and should be replaced with the specific molecule, receptor, or enzyme involved.

Other names

Pro-inflammatory pathwaysInflammatory signaling pathwaysInflammation-related pathwaysInflammatory cascades

Inhibition of signal transduction (e.g., blocking NF-κB activation, JAK-STAT phosphorylation); Inhibition of receptor activation (blocking TLRs or cytokine receptors); Promotion of endogenous negative regulators (anti-inflammatory cytokines, signal suppressors)