Fig. 2

Potential mechanism of MSCs in the treatment of BLM-induced lung injury. ①MSCs reduce BLM-induced epithelial cell necrosis or apoptosis by inhibiting oxidative stress response, and further reduce the production of inflammatory mediators such as cytokines and chemokines. MSCs promote the expression of TLR-4 in alveolar epithelial cells, trigger the lung regeneration signal of HA-TLR-4, and promote the regeneration and repair of alveolar epithelial cells. ② Immunomodulatory effects of MSCs: MSCs reduce the expression and density of CD80 costimulatory molecules in macrophages and dendritic cells, and reduce their ability to induce antigen-specific T cell immune response; MSCs promote the transformation of macrophages to M2 phenotype, reduces the inflammatory potential, and increases the synthesis and secretion of MMP-9, which contributes to the degradation of extracellular matrix, including collagen; MSCs reduce macrophages and dendritic cells the expression of chemokine (lymphotoxin, CCL21, CXCL12, CXCL13), thus reducing the B cells to recruit; ③Direct induction of apoptosis of activated T cells through Fas/FasL signaling pathway alleviates abnormal excessive immune response; ④ MSCs inhibit epithelial mesenchymal transformation (EMT); ⑤ MSCs inhibit the activation of TGF-β/SMAD-3 signaling pathway, thus inhibiting the activation of myofibroblasts and further reducing the synthesis of collagen and other extracellular matrix (ECM)