Abstract
Purpose: Alpha 7 acetylcholine nicotinic receptor (α7nAChR) (composed of 5 α7 subunits encoded by Chrna7 gene) activation by endogenous (Ach) or exogenous ligand (nicotine) attenuates inflammation, including in osteoarthritis (OA). Therefore, enhancing α7nAChR signaling might be a potential therapeutic target for OA. However, during evolution a human specific partial duplicate of chrna7 called CHRFAM7A has emerged, and it is expressed in 75% of the population. It functions as a dominant negative of α7nAChR and may decrease α7nAChR signaling and agonist efficiency in OA.
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