HIF1A and cerebral infarction: Since HIF-1α-induced NOX2 activation underlies microvascular endothelial cell destruction during cerebral infarction, HSYA rescues cerebrovascular ECs from endotoxin damage by inhibiting the HIF-1α/NOX2 signaling cascade and increasing ZO-1 expression, which is primarily due to the protection of redox homeostasis, a finding that suggests a potential clinical application of HSYA in cerebrovascular protection (Li Y. et al., 2022).