Abstract:

Organ structure destruction and functional decline leading to failure due to fibrosis pose severe threats to the human health and life. Macrophages are important immune cells present in various tissues and organs. Under the influence of numerous factors and pathways， such as transforming growth factor-β1（TGF-β1）， Toll-like receptor 4（TLR4）/nuclear factor-κB（NF-κB）， Janus kinase（JAK）/signal transducer and activator of transcription（STAT）， Notch signaling pathway， peroxisome proliferator-activated receptor（PPAR）， and cAMP response element-binding protein（CREB）， the macrophages may undergo polarization. In visceral organ fibrosis， the macrophage polarization signaling network， composed of single or multiple factors and pathways， is one of the crucial mechanisms regulating fibrosis. After polarization， the macrophages produce the chemokines and matrix metalloproteinase（MMP）， which are related to promoting fibrosis， leading to the occurrence and development of fibrosis. The current research conducted domestically and internationally mainly focuses on the roles of macrophages in infection， tumors， and fibrosis， with few summaries on the mechanisms of macrophage polarization in fibrosis. This review summarizes the pathways involved in macrophage polarization and the mechanisms of macrophage polarization in organ fibrosis， and provide the basis for the targeted therapy of fibrosis.

Key words: Fibrosis, Macrophage polarization, M1 macrophage, M2 macrophage, Signaling pathway