Targeting cardiac fibrosis with chimeric antigen receptor macrophages
Zibei Gao, Lei Yan, Jufeng Meng, Zhengkai Lu, Kaixin Ge, Zhen Jiang, Teng Feng, Haopeng Wang, Chen Liu, Juan Tang, Hui Zhang
Abstract
Cardiac fibrosis, a significant global health issue associated with nearly all forms of heart disease, is characterized by excessive extracellular matrix (ECM) deposition within the myocardium, leading to reduced tissue compliance and accelerating the progression to heart failure 1 . In response to myocardial injury, resident cardiac fibroblasts are recruited to injured zones, where they become highly activated fibroblasts (myofibroblasts), enhancing the secretion of ECM proteins 2 . Genetic ablation of myofibroblasts following injury reduces ECM production, alleviates cardiac fibrosis, and improves heart function 3 , 4 . However, clinical interventions and therapies targeting cardiac myofibroblasts remain limited.