Icariin diminishes the enzymatic activity of PDE5A and significantly prevents mitochondrial dysfunction and the autophagy process, thereby leading to cardioprotective effects.34 In addition, the principal active constituents of SMYAD retrain autophagy by inhibiting PDE5A, thereby modulating the AKT/mTOR/ULK1 pathway in isoproterenol-induced heart failure.33 Here, we identified PDE5A as one of the potent targets of the MEX3A/circMPP6 complex during CRC progression and proposed a crucial PBs-dependent mechanism for PDE5A mRNA degradation in CRC. Here, MTOR is linked to heart failure.