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Sildenafil for treatment of lung fibrosis and pulmonary hypertension: a randomised controlled trial
Sildenafil causes preferential pulmonary vasodilation and improves gas exchange in patients with severe lung fibrosis and secondary pulmonary hypertension, and ratio of pulmonary to systemic vascular resistance decreased only in individuals who received nitric oxide and sildanafil. Expand
WNT1-inducible signaling protein-1 mediates pulmonary fibrosis in mice and is upregulated in humans with idiopathic pulmonary fibrosis.
This study identifies WISP1 as a key regulator of ATII cell hyperplasia and plasticity as well as a potential therapeutic target for attenuation of pulmonary fibrosis. Expand
Combination Therapy with Oral Sildenafil and Inhaled Iloprost for Severe Pulmonary Hypertension
This randomized, controlled trial of low- or high-dose sildenafil, with or without inhaled iloprost, showed dose-dependent improvement in mean pulmonary artery pressure and hemodynamics with sildanafil alone, and phosphodiesterase-5 inhibitors in combination with inhaled prostanoid during right-heart catheterization. Expand
Sildenafil for long-term treatment of nonoperable chronic thromboembolic pulmonary hypertension.
After approximately 6 months of sildenafil treatment, pulmonary hemodynamics and exercise capacity improved significantly and oral sildinafil may offer a new option for medical treatment of this devastating disease. Expand
Oral sildenafil as long-term adjunct therapy to inhaled iloprost in severe pulmonary arterial hypertension.
In patients with severe PAH deteriorating despite ongoing prostanoid treatment, long-term adjunct oral sildenafil improves exercise capacity and pulmonary hemodynamics. Expand
NOX4 regulates ROS levels under normoxic and hypoxic conditions, triggers proliferation, and inhibits apoptosis in pulmonary artery adventitial fibroblasts.
NOX4 maintains ROS levels under normoxic and hypoxic conditions and enhances proliferation and inhibits apoptosis of PAFB and a significant increase of NOX4 mRNA expression was observed under hypoxic Conditions in PAFB from the lungs with IPAH compared to healthy donors. Expand
The angiotensin II receptor 2 is expressed and mediates angiotensin II signaling in lung fibrosis.
It is concluded that ANGII signaling occurs primarily via AGTR1 in normal fibroblasts, while AGTR2-mediated effects are dominant on activated (myo)-fibro Blasts, a receptor switch that may perturb epithelial-mesenchymal interaction, thereby further perpetuating fibrogenesis. Expand
Upregulation of NAD(P)H oxidase 1 in hypoxia activates hypoxia-inducible factor 1 via increase in reactive oxygen species.
It is concluded that hypoxic upregulation of Nox1 and subsequently augmented ROS generation may activate HIF-1-dependent pathways. Expand
HIF-1 alpha signaling is augmented during intermittent hypoxia by induction of the Nrf2 pathway in NOX1-expressing adenocarcinoma A549 cells.
Fluctuations in cellular oxygenation causing intermittent hypoxia and oxidative stress affect the regulation of hypoxia-inducible factor (HIF-1) and the nuclear factor erythroid 2-related factor 2Expand
The listerial exotoxins listeriolysin and phosphatidylinositol-specific phospholipase C synergize to elicit endothelial cell phosphoinositide metabolism.
It is concluded that the listerial exotoxins LLO and PIcA cooperate to provoke potent second messenger synthesis in endothelial cells, in the absence of cell invasion by the bacteria. Expand