A sample of the latest PH news output from around the web for your reference.
Inhibition of Shp2 Protein Eases Pulmonary Arterial Hypertension Symptoms in Rats, Study Reports
The study, “Inhibition of Shp2 ameliorates monocrotaline-induced pulmonary arterial hypertension in rats,” was recently published in BMC Pulmonary Medicine.
Treatment with Phps-1, which inhibits a protein called Shp2, was able to alleviate specific symptoms of pulmonary arterial hypertension (PAH) in a rat model, suggesting that Shp2 may be a potential therapeutic target for PAH treatment.
BET Proteins Could Be Therapeutic Target for COPD Patients with PH, Rat Study Suggests
Inhibition of proteins that regulate gene expression — called BET — were found to ease pulmonary hypertension (PH) in a rat model of chronic obstructive pulmonary disease (COPD), a study reports.
The study, “Inhibition of BET Proteins Reduces Right Ventricle Hypertrophy and Pulmonary Hypertension Resulting from Combined Hypoxia and Pulmonary Inflammation,” appeared in the International Journal of Molecular Sciences.
Clinical Trial Expected in 2019 to Test Therapy C76 as Potential PAH Inhibitor
A clinical trial to study a therapy that may inhibit and possibly reverse vascular remodeling in pulmonary arterial hypertension (PAH) is expected to start enrolling patients in 2019.
The medicine, C76, was shown to inhibit a gene called HIF-2α and to lead to reversal of PAH in animal models.
The study reporting the findings, “Therapeutic Targeting of Vascular Remodeling and Right Heart Failure in PAH with HIF-2α Inhibitor,” was published in the American Journal of Respiratory Critical Care Medicine.
Drug identified that could reverse pulmonary arterial hypertension
Findings originally published in the American Journal of Respiratory Critical Care Medicine, identify a safe drug that for the first time could treat – and possibly reverse – the thickening of lung artery walls in pulmonary arterial hypertension; clinical trial is expected in 2019.
Scientists at Stanley Manne Children's Research Institute at Ann & Robert H. Lurie Children's Hospital of Chicago took a major step toward developing a new treatment for pulmonary arterial hypertension (PAH), a severe lung disease with a five-year survival rate of 50 percent. They identified a drug with a positive safety profile that inhibits a gene called HIF-2α, which they discovered earlier promotes the progressive thickening of the lung artery walls - a key feature of PAH called "vascular remodeling," which leads to right-sided heart failure, the main cause of death in PAH patients.
Anti-cancer Therapy Sorafenib Reverses PAH in Rat Model, Study Reports
Research & development treatment with the approved anti-cancer medication sorafenib reversed pulmonary arterial hypertension (PAH) and cardiopulmonary remodeling (CPR) in a rat model, according to a new study. The findings suggest that a low-dose therapy with this compound may be successful in PAH treatment, the Japanese research team suggests.
Tenascin-C Is Induced With Progressive Pulmonary Vascular Disease in Rats and Is Functionally Related to Increased Smooth Muscle Cell Proliferation
Abstract from 'Circulation Research':
Tenascin-C, an extracellular matrix glycoprotein prominent during tissue remodeling, has been linked to cell migration, proliferation, and apoptosis. To determine its potential role in the pathobiology of pulmonary hypertension, we compared tenascin expression in adult and infant rat pulmonary arteries (PAs) after injection of the toxin monocrotaline. Immunohistochemistry, in situ hybridization, and Northern blot analysis demonstrated induction of tenascin in adult rat central and peripheral PA. Tenascin was not, however, detected in infant vessels, which show spontaneous regression of vascular lesions. To determine a function for tenascin, we correlated its expression with evidence of apoptosis and cell proliferation using the TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay and 5-bromo-2′-deoxyuridine labeling, respectively. Apoptosis was observed only in the adult rat PA endothelial cell layer, preceding the induction of tenascin, which colocalized both temporally and spatially with proliferating smooth muscle cells (SMCs). A cause-and-effect relationship was documented in cultured rat PA SMCs, where tenascin promoted growth in response to basic fibroblast growth factor and was a prerequisite for epidermal growth factor–induced proliferation. These data provide novel functional information suggesting that endothelial cell apoptosis precedes progressive pulmonary hypertension and that induction of tenascin may be critical to growth factor–dependent SMC proliferation.