ArticleTranslational neurodegeneration2026
Capsaicin suppresses microglial inflammation through TRPV1-SSR4 interaction.
Article in Translational neurodegeneration, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundTransient receptor potential vanilloid 1 (TRPV1) is increasingly recognized as an important regulator of microglial response during neuroinflammation, a key pathological feature of various neurodegenerative diseases such as Alzheimer's disease. Capsaicin, the primary pungent component in chili peppers, executes its anti-inflammatory properties as a TRPV1 agonist. Although the mechanism of TRPV1 channel activation and signal transduction by capsaicin has been extensively studied, the protein-protein interaction-based mechanisms by which TRPV1 modulates microglial inflammatory responses in the context of neurodegeneration remains unclear.
methodsWe used a lipopolysaccharide-induced acute neuroinflammation model to examine the effects of TRPV1 activation and pharmacological blockade of TRPV1 channel gating on microglial inflammatory responses. Proximity labeling-based proteomics, bioluminescence resonance energy transfer, and NanoLuc Binary Technology were used to identify and characterize TRPV1-interacting proteins. Signal sequence receptor subunit 4 (SSR4) knockdown and forced interaction between TRPV1 and SSR4 were performed to assess the functional contribution of the TRPV1-SSR4 interaction. Structural modeling, BRET-based domain mapping, and colocalization analyses were further used to examine the molecular and subcellular features of SSR4 recruitment by TRPV1.
resultsIn the neuroinflammatory model, the TRPV1 agonist capsaicin attenuated pro-inflammatory cytokine production, neuronal apoptosis, microgliosis, and microglial soma enlargement in a TRPV1-dependent manner. Notably, pharmacological blockade of TRPV1 channel gating by capsazepine did not abolish the anti-inflammatory action of capsaicin, suggesting an alternative mechanism of action beyond the canonical ligand-gated Ca
conclusionsOur findings suggest that capsaicin suppresses microglial inflammation mediated by the TRPV1-SSR4 interaction, providing new insights into the chemical biology basis of TRPV1 interoceptive signaling and potential applications of natural TRPV1 agonists for modifying therapy of neuroinflammation-associated neurodegeneration.
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