Figure 9.

The axis TGF‐β1/miR‐382‐5p/SOD2. The axis TGF‐β1/miR‐382‐5p/SOD2 as mechanism underlying the overproduction of ROS in CD34+ PMF cells. ROS level could increase as a consequence of: (a) the release of pro‐inflammatory cytokines from granulocytes induced by miR‐382‐5p overexpression; (b) the enhanced expression of miR‐382‐5p, which reduces the expression of its target SOD2; (c) the upregulation of miR‐382‐5p by TGF‐β1. The TGF‐β‐receptor I kinase inhibitor galunisertib could inhibit the production of ROS by reducing the expression level of miR‐382‐5p and restoring SOD2 activity.