Inhibition of HO with 1J or sGC with ODQ prevented this effect, confirming that heme decreases detrusor contractility through activation of the HO–CO–sGC–cGMP pathway, reproducing a functional pattern similar to that observed in SCD, where excessive intravascular hemolysis leads to elevated circulating heme and bladder hypocontractility [32,50]. The gene discussed is AQP1; the disease is Schnyder corneal dystrophy.