On December 15, the reporter learned from Liangzhu Laboratory that the research team of Zhang Jin, a researcher in the laboratory, and the research team of Song Mozhi, a doctor from the Institute of Zoology, Chinese Academy of Sciences, reported for the first time the application potential of targeted chimeric antigen receptor macrophage therapy in the treatment of tissue damage and fibrosis caused by myocardial ischemia/reperfusion. The relevant paper was recently published in the international academic journal "Circular Research". Myocardial ischemia-reperfusion injury is a serious complication after the treatment of ischemic heart disease, which has a significant impact on the prognosis and survival rate of myocardial infarction patients, and the current treatment methods are limited. Cardiac fibrosis is a common pathological change after myocardial ischemia-reperfusion injury. Excessive fibrosis can damage the structure of the heart and impair its systolic and diastolic functions, ultimately leading to heart failure. In recent years, scientists have attempted to improve myocardial fibrosis related to ischemia-reperfusion injury by inhibiting the activity of pro fibrotic factors and promoting the degradation of collagen fibers. However, there is currently a lack of effective clinical intervention methods. In cardiac fibrosis diseases such as myocardial ischemia-reperfusion injury, fibroblast activation protein (FAP) is highly expressed in activated fibroblasts. In response to tissue damage, fibroblasts undergo a dynamic transition from fibroblasts to myofibroblasts. Transient activation of myofibroblasts contributes to tissue repair, but sustained activation can lead to pathological fibrosis. Through mouse experiments, the research team found that from the third day after myocardial ischemia-reperfusion injury, the number of FAP positive myofibroblasts in the mouse heart significantly increased. Based on this, the research team constructed FAP CAR-Ms macrophages with targeted FAP function. In a mouse model of myocardial ischemia-reperfusion injury, the research team found that intravenous injection of FAP CAR Ms on the third day after surgery significantly improved mouse cardiac function and reduced the degree of myocardial fibrosis. Through experiments, it has been confirmed that FAP CAR Ms can migrate to the site of myocardial injury and target the phagocytosis of FAP positive myofibroblasts, thereby reducing the proportion and quantity of myofibroblasts in the damaged heart. In addition, the research team also conducted a systematic evaluation of the safety of FAP CAR Ms treatment, preliminarily confirming the safety of this therapy. The tracking results showed that FAP CAR Ms still had a protective effect on mouse cardiac function after 3 months of myocardial ischemia-reperfusion injury. Zhang Jin introduced that this study demonstrated the role of FAP CAR Ms therapy in reducing myocardial fibrosis and protecting heart function, and provided new ideas for the treatment of other cardiovascular diseases with fibrotic phenotypes. (New Society)