MEX3B leads to aberrant expression of VCAN, aggravating the thoracic aortic dissection by contributing to the phenotype transformation of VSMCs

, small interfering RNA pool‑mediated MEX3B downregulation triggered VSMC switching from a synthetic towards a contractile phenotype. High‑throughput transcriptomics demonstrated that the MEX3B knockdown reduced the expression of versican (VCAN). MEX3B potentiated VCAN mRNA stability by binding to its 3'untranslated region. VCAN downregulation induced a contractile phenotype of VSMCs. In conclusion, the loss of MEX3B protected against TAD, potentially via its contribution to VSMC phenotype switching, which may be associated with the downregulation of VCAN. The present study preliminarily demonstrated the function and mechanism of MEX3B in TAD. These findings provide a theoretical basis for understanding TAD pathogenesis.