Fig. 2

After kidney injury, the microenvironment would turn to be inflammatory, hypoxic, and immunostimulatory. The proinflammatory microenvironment induced by neutrophil granulocyte and mononuclear macrophage infiltration leads to the massive release of injurious factors such as TGF-β, IFN-γ, IL-6, and so on. This will recruit stem/progenitor cells through the interaction between SDF-1 and CXCR4/7, HA/osteopontin and CD44, and others. In addition, the insufficient oxygen supply caused by ischemia and increase in oxygen consumption in the disease state would certainly result in the hypoxic microenvironment. This would aid to the recruitment and differentiation of stem/progenitor cells and induce the production of lots of angiogenesis factors in these cells to facilitate tissue repair. The immune responses include the activation of B cells, T cells, NK cells, and dendritic cells, which constructs the local immune microenvironment to affect the stem/progenitor cell-induced tissue repair. Overall, the various factors in the local microenvironment build up an intricate network to cooperatively assist stem/progenitor cell functions and finally promote stem/progenitor cell-dependent tissue repair through their beneficial effects on angiogenesis, anti-inflammation, immunosuppression, and others