Research advances on the mechanism of macrophage polarization in renal interstitial fibrosis

Renal interstitial fibrosis (RIF) is a common pathological process for many chronic kidney diseases (CKD). As heterogeneous cells capable of promoting the occurrence and development of RIF, macrophages are the major driving factors of end-stage renal disease (ESRD). Although its pathogenic role in renal inflammation and fibrosis is widely recognized, it also plays some key role in tissue remodeling, repairing and immune regulation. Under the stimulation of microenvironment, macrophages may polarize into various phenotypes (mainly M1 & M2), thus exerting pro-inflammatory and anti-inflammatory effects. Recent studies have confirmed that these two phenotypes may regulate inflammation and promote tissue repair in chronic kidney diseases, acting as potential therapeutic targets of RIF. Therefore understanding the role of different macrophage phenotypes during renal injury and repair is vital for elucidating molecular mechanism and a proper treatment of RIF. Furthermore, the exact role of macrophages in various aspects of RIF should be further explored.