Fig. 9
Mechanism of tRF-Glu-CTC promotion of neointimal hyperplasia. After vascular wall injury, TGF-β1 is produced by the recruitment of inflammatory cells (neutrophils/macrophages, etc.), which is a potent agonist of vascular smooth muscle cells and mediates neointimal formation by promoting proliferation and migration of VSMCs via Smad3. Vascular injury induced the expression of tRF-Glu-CTC, which suppressed fibromodulin (FMOD) levels through the RNA silencing mechanism. FMOD is a TGF-β1 antagonist that inhibits the activity of TGF-β1. Thus, tRF-Glu-CTC played a promoting role in the process of neointima formation by indirectly facilitating the activity of TGF-β1