Sildenafil, primarily known for its role in treating erectile dysfunction, inhibits phosphodiesterase type 5 (PDE5). This enzyme breaks down cyclic guanosine monophosphate (cGMP), a crucial molecule for vasodilation. By blocking PDE5, sildenafil increases cGMP levels, leading to smooth muscle relaxation and improved blood flow.
In pulmonary fibrosis (PF), reduced blood flow and vasoconstriction contribute to disease progression. Sildenafil’s vasodilatory effects may therefore offer therapeutic potential. Preclinical studies show sildenafil can improve pulmonary artery pressure and reduce right ventricular hypertrophy in animal models of PF. Some human studies suggest potential benefits in improving exercise capacity and reducing dyspnea in patients with PF associated pulmonary hypertension. However, larger, well-designed clinical trials are needed to confirm these findings and establish optimal dosing strategies.
Researchers are investigating sildenafil’s potential effects beyond vasodilation. It might also influence inflammation and fibrosis, key processes driving PF. Studies explore sildenafil’s interaction with other signaling pathways involved in PF pathogenesis, suggesting potential for broader therapeutic impact.
While promising, research remains ongoing to fully understand sildenafil’s role in PF treatment. Current evidence warrants further investigation to define its precise role, determine appropriate patient selection criteria, and assess its long-term effects and potential side effects.
