LRG1 is linked to increased brain infarct volume, enhanced autophagy, and apoptosis of brain cells, thereby contributing to the aggravation of cerebral ischemia–reperfusion injury.50,51 Experimental rodent work has shown that LRG1 silencing may alleviate intracranial status following sepsis-associated encephalitis.52 This indicates that LRG1 is a potentially important molecule in both ischemic-related injuries and infection-driven inflammation in the brain. Here, LRG1 is linked to Cerebral ischemia.