Reducing Upstream Compliance Induces Downstream High Pulsatility Flow-Dependent Inflammatory Response in Pulmonary Endothelial Cells via TLR2/NF-KB Pathway

Pulmonary arterial hypertension (PAH) is a group of chronic, progressive and fatal diseases, characterized by the dysfunction of the small arteries and microvasculature in the pulmonary circulation. Due to high blood pressure and high resistance in the pulmonary arteries, PAH causes detrimental damage on the lung and right heart ventricle. If left untreated, PAH quickly becomes life threatening. Although the exact pathophysiology remains unknown, there is increasing evidence suggesting that inflammation likely plays an important role in inducing and perpetuating the PAH progress. Although anti-inflammatory therapy has been shown effective in certain connective-tissue-disease-associated PAH, this approach has not been tested in other PAH conditions. The potential benefit of anti-inflammatory therapy to treat various PAH conditions could be of importance and require further study on the possible pathological mechanisms underlying the therapeutic effects.