Acute hypoxia activates TRPA1 channels in cerebral artery endothelial cells to activate an early adaptive response to reduce tissue ischemic damage through vasodilation.

The combination of NSCs with NSC-derived exosomes ameliorated the injury of brain tissue including cerebral infarction, neuronal death, and glial scarring, and promoted the recovery of motor function.

An RNAi screen in mouse hippocampal neuronal cell line targeting epigenetic regulators revealed a novel neuroprotection of Prmt5 and uncovered its nucleus translocation feature and epigenetic mechanism in cerebral ischemia.

Functional ultrasound imaging was used to monitor brain hemodynamics and sensory-evoked thalamocortical functions in awake rats pre- and post-stroke, advancing our understanding toward new therapeutic developments.

The kinase JNK is required in endothelial cells for the development of native collateral arteries.

An interaction between the ion channel ASIC1a and the protein RIP1 is responsible for neuronal death caused by tissue acidosis.

The UPOAO model effectively replicates retinal ischemia in retinal artery occlusion, providing a novel platform for identifying pathogenic genes and advancing therapeutic research.

Machine learning models effectively predict the risk of post-stroke epilepsy using extensive clinical data, offering new insights for improving patient management in clinical neurology.

A new tracer infusion method is used to confirm that pulsatile cerebrospinal fluid transport into the brain occurs naturally and is driven by the cardiac cycle, not by tracer injection.