巨噬细胞
转化生长因子
生长因子
心室重构
生物
信号转导
细胞生物学
癌症研究
免疫学
内科学
医学
凝结
心肌梗塞
受体
生物化学
体外
作者
Venkata Garlapati,Qi Luo,Jens Posma,M Aluia,Than Son Nguyen,Kristin Grunz,Michael Molitor,Stefanie Finger,Gregory S. Harms,Tobias Bopp,Wolfram Ruf,Philip Wenzel
标识
DOI：10.1161/circresaha.123.324114
摘要
Excess fibrotic remodeling causes cardiac dysfunction in ischemic heart disease, driven by MAP (mitogen-activated protein) kinase-dependent TGF-ß1 (transforming growth factor-ß1) activation by coagulation signaling of myeloid cells. How coagulation-inflammatory circuits can be specifically targeted to achieve beneficial macrophage reprogramming after myocardial infarction (MI) is not completely understood.
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