These findings support a model in which HMGB1 and CGRP participate in a positive neuron-endothelial feedback loop under inflammatory and hypoxic stress, potentially amplifying neurovascular signaling relevant to migraine. Although derived from an in vitro system, this study identifies HMGB1 as a potential upstream modulator of CGRP-associated pathways and highlights its possible contribution to peripheral mechanisms involved in trigeminovascular activation.
Song et al. (Sat,) studied this question.