Figure 1.
The proposed pathway by which circTLK1 regulates stroke progression. Upregulated circTLK1 directly binds to miR-335-3p and acts as an endogenous miR-335-3p sponge to inhibit miR-335-3p activity and concomitantly increase the expression of the downstream intermediate TIPARP, which results in neuronal injury and contributes to cerebral infarction and neurological deficit. ceRNA, competing endogenous RNA.