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. 2021 May 18;22(10):5323. doi: 10.3390/ijms22105323

Figure 7.

Figure 7

Proposed network of miR-143-5p–CRIM1 autophagy in regulating endometrial receptivity. Our results suggest that hormones and IFN-τ promote CRIM1 expression by inhibiting the level of miR-143-5p, while CRIM1 regulates endometrial receptivity phenotypes through autophagy activation to reduce the production of ROS.