The reporter learned on August 11 that Liu Qiang, a professor at the General Hospital of Tianjin Medical University, found that the damaged brain tissue after stroke can continuously activate vascular endothelial cells, leading to adhesion of myeloid cells such as monocytes, thus accelerating atherosclerosis after stroke and increasing the risk of stroke recurrence. The research paper was published in the international journal "Immunology". Stroke, commonly known as stroke, is an acute cerebrovascular disease and one of the leading causes of death and disability among adults in China. Data shows that up to 40% of outpatient stroke patients in China are recurrent populations. According to statistics, 17.1% of patients will experience a recurrence of stroke or other vascular events within one year after stroke, and the recurrence rate exceeds 30% within five years. Even with secondary preventive treatment, 3% to 6% of patients still experience recurrence 3 months after stroke. Compared to non recurrent patients, stroke recurrence increases the risk of disability or death by approximately 9.4 times. Clarifying the residual risk of stroke recurrence and promoting the translation of research evidence into clinical practice is of great significance for stroke prevention and treatment. The research team found that lumen stenosis caused by atherosclerosis, embolism caused by plaque shedding and small vessel occlusion were the main factors leading to recurrence of stroke within 3 months after onset. Through techniques such as positron emission tomography (PET-CT), two-photon imaging, and single-cell sequencing, the team observed that cerebral ischemia caused sustained activation and aging of peripheral vascular endothelial cells in patients, which upregulated the level of immune adhesion molecule VCAM1, leading to a significant increase in monocyte and neutrophil adhesion. The detection of stroke patient samples found that the damaged brain tissue after stroke can continuously release the Notch1 receptor ligands DLL1 and Jagged1 through the exocrine body, activate the Notch1 pathway of peripheral vascular endothelial cells, cause vascular inflammation, accelerate atherosclerosis and stroke recurrence. Blocking adhesion molecule VCAM1 or Notch1 receptor with antibody drugs can delay atherosclerosis after stroke. On this basis, the research group proposed a new strategy to predict the progression of atherosclerosis after stroke by evaluating the peripheral blood DLL1 and Jagged1 of stroke patients, and a new concept to delay the progression of atherosclerosis after stroke through immune intervention targeting the adhesion molecules VCAM1 and Notch1 receptor. (New Society)