Figure 8.

Proposed Model for Sal-miR-58-Induced Autophagy and Anti-inflammation in VSMCs

Sal-miR-58 enters VSMCs after exogenous administration and downregulates KLF3 expression through direct binding to the 3′ UTR of KLF3 mRNA, which in turn relieves KLF3 repression of NEDD4L expression, rendering upregulated NEDD4L expression. Increased NEDD4L facilitates the ubiquitination and degradation of PFKP, leading to a decrease in the activation of Akt/mTOR signaling and thus resulting in induction of VSMC autophagy.