HEA ameliorates gastric dysmotility in DGP by suppressing the cGAS-STING pathway, attenuating M2 macrophage pyroptosis and inflammatory responses, and preserving ICC networks. These findings identify a novel EA/cGAS-STING/pyroptosis axis and highlight its therapeutic potential as a mechanistic target for optimizing DGP treatment strategies.
Fan et al. (Fri,) studied this question.