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Experimental study demonstrates that FHF2 overexpression dampens DRG neuronal excitability in inflammatory pain models, suggesting potential therapeutic utility for pain management.
FHF2 is known to bind to and modulate the function of Nav1.7. FHF2 expression is also reduced after nerve injury. We demonstrate that knockdown of FHF2 expression increases DRG neuronal excitability. More importantly, overexpression of FHF2 reduces DRG excitability in basal conditions and in the presence of inflammatory mediators (a model of inflammatory pain). These results suggest that FHF2 could potentially be used as a tool to reduce DRG neuronal excitability and to treat pain.
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Effraim et al. (2022) studied this question.
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