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European Respiratory Journal 10/10/2019 03:05
Macrophages are major players in the pathogenesis of pulmonary arterial hypertension (PAH). To investigate whether lung macrophages and pulmonary-artery smooth muscle cells (PASMCs) collaborate to stimulate PASMC growth and whether the CCL2-CCR2 and CCL5-CCR5 pathways inhibited macrophage–PASMC interactions and PAH development, we used human CCR5-knock-in mice and PASMCs from patients with PAH and controls. Conditioned media from murine M1 or M2 macrophages stimulated PASMC growth.
European Respiratory Journal 09/12/2019 03:30
The adaptation of right ventricular (RV) systolic function to afterload is a major determinant of outcome in pulmonary hypertension [1]. The gold standard measurement of RV–pulmonary arterial (PA) coupling is the ratio of end-systolic to arterial elastances ( E es / E a ) which is optimal for RV flow output at minimal energy cost at values between 1.5 and 2 [2]. Progressive RV–PA uncoupling is associated with maintained RV dimensions down to E es / E a values of around 0.8 [3]. Thus, the evaluation of RV–PA coupling would theoretically allow monitoring of the transition from compensated to decompensated RV function in pulmonary hypertension. However, measuring RV–PA coupling at the bedside is technically demanding and invasive.
European Respiratory Journal 08/22/2019 03:30
Pulmonary arterial hypertension (PAH) is a progressive disease mainly characterised by a widespread obstruction of distal pulmonary arteries [1]. Untreated, this disease rapidly leads to right heart failure, then to death [2]. Heritable PAH (hPAH) represents about 30% of PAH cases, and this category includes familial forms with or without identified mutations, and sporadic forms carrying a mutation. The first genetic abnormalities discovered in hPAH were bone morphogenetic protein receptor-2 ( BMPR2 ) mutations. Loss of function of this receptor results in proliferation of vascular smooth muscle cells and selection of endothelial cell clones resistant to apoptosis [3]. Since, several other mutations have been implicated in PAH. Mutation in
European Respiratory Journal 08/22/2019 03:30
Introduction. Pulmonary arterial hypertension (PAH) is one of the leading causes of mortality in systemic sclerosis (SSc). We explored the impact of the updated haemodynamic definition of pulmonary hypertension (PH), as proposed by the 6th World Symposium on Pulmonary Hypertension. Methods. In this single-centre retrospective analysis, patients with SSc who had right heart catheterisation (RHC) were included. We compared the prior PH definition to the updated PH definition. The prior definition classified PH as mean pulmonary arterial pressure (mPAP) ≥25 mmHg and further divided into pre-capillary PH (PAH and PH due to lung disease and/or hypoxia), post-capillary PH, and combined pre- and post-capillary PH groups. For the updated definition,
European Respiratory Journal 08/22/2019 03:30
The introduction of the new haemodynamic definition of pulmonary hypertension (PH) was admittedly the most significant and controversial recommendation of the 6th World Symposium on Pulmonary Hypertension (WSPH) [1]. According to the previous definition, PH was limited to levels of mean pulmonary arterial pressure (mPAP) ≥25 mmHg, whereas the new definition closed the gap to the upper level of physiological mPAP and included values ≥21 mmHg for both pre- and post-capillary PH (table 1) [2]. Since the WSPH conference in 2018, there have been arguments for and against the new definition in the scientific community, and recent editorials in the European Respiratory Journal urged further analysis of large databases in order to understand the "r.
European Respiratory Journal 08/01/2019 03:05
Pulmonary arterial hypertension (PAH) is a progressive fatal disease characterised by abnormal remodelling of pulmonary vessels, leading to increased vascular resistance and right ventricle failure. This abnormal vascular remodelling is associated with endothelial cell dysfunction, increased proliferation of smooth muscle cells, inflammation, and impaired bone morphogenetic protein (BMP) signalling. Orphan nuclear receptor Nur77 is a key regulator of proliferation and inflammation in vascular cells, but its role in the impaired BMP signaling and vascular remodelling in PAH is unknown. We hypothesised that activation of Nur77 by 6-mercaptopurine would improve the PAH by inhibiting endothelial cell dysfunction and vascular remodelling. Nur77

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