Comment on "Hyperglycemia-triggered STAT3 activation drives thromboinflammation via NETs formation to promote hemorrhagic transformation after stroke".

This correspondence provides a critical perspective on the recent study by Zhao et al. defining the hyperglycemia-STAT3-neutrophil extracellular trap-thromboinflammation axis in post-ischemic stroke hemorrhagic transformation. Beyond three core unresolved scientific gaps concerning cell-type specificity, tissue plasminogen activator-associated pathological context, and glycemic model heterogeneity, we extend the discussion to supplementary translational constraints, the upstream regulatory role of mitochondrial oxidative stress, and implications for clinical trial design. These viewpoints aim to further enhance the translational potential of this promising therapeutic target.