Nicotinic acetylcholine receptors: Therapeutic targets for novel ligands to treat pain and inflammation.
Level 5 - mechanism / opinion, no new human data
Narrative review without systematic methodology (mechanism-based reasoning)
PubMed 36868367 · doi:10.1016/j.phrs.2023.106715
What was done
This narrative review synthesizes research on the role of nicotinic acetylcholine receptor (nAChR) subtypes (specifically those containing α7, α9, and/or α10 subunits) in modulating pain and inflammation through the cholinergic anti-inflammatory pathway, and surveys recent progress in novel ligand development.
What was found
The abstract reports no numerical findings or effect sizes. It qualitatively describes that nAChRs mediate non-ionic signaling pathways in immune cells, can be activated by endogenous ligands other than acetylcholine and choline, and serve as targets for developing therapeutic ligands.
Why it matters
It highlights the therapeutic potential of targeting non-ionic nAChR signaling pathways in immune cells to develop new classes of non-opioid anti-inflammatory and analgesic treatments.
Limits
As a narrative review, there is no systematic search protocol, risk of bias assessment, or quantitative data synthesis. The abstract provides no primary human clinical data or safety and efficacy metrics.
Cited by
- supports No nicotine is naturally produced in the human body; the endogenous ligand for the nicotinic acetylcholine receptor is acetylcholine.