Pain mediators

"Pain mediators" is a descriptive label for the diverse group of molecules—including cytokines (e.g., interleukins, TNF-α), chemokines, neurotransmitters (e.g., glutamate, substance P, serotonin), growth factors (e.g., nerve growth factor), eicosanoids (e.g., prostaglandins), ion channels (e.g., TRPV1, sodium channels), and their receptors—that activate, sensitize, or modulate nociceptive neurons and thus participate in the physiological and pathological processes of pain perception[1][2][3][4][5][6][7]. This term is not specific to any single molecular target and cannot be mapped to a unique gene, protein, or receptor; it instead refers to the overall molecular machinery underpinning pain signaling in health and disease. Important Note: "Pain mediators" is not a canonical, singular molecular entity and cannot be mapped to a unique gene/protein/receptor entry. Instead, it represents a functional category. For structured data curation, use individual mediator names (e.g., "Prostaglandin E2", "Nerve growth factor", "Interleukin-6") as canonical targets.

Other names

pain signaling moleculespain pathway mediatorsnociceptive mediatorsalgogenic substancespronociceptive mediators

Mechanisms are specific to the mediator and drug, including: Inhibition of prostaglandin synthesis; Blockade of ion channels; Antagonism/agonism at neurotransmitter receptors; Inhibition of cytokine signaling.