An in vitro study reveals HMGB1 enhances neurovascular signaling in the trigeminovascular system, suggesting new migraine pathways.
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.
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Song et al. (2026) studied this question.
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