Ingrid Schalij

Pneumonectomy combined with SU5416 or monocrotaline pyrrole does not cause severe pulmonary hypertension in mice

Xiao‐Qing Sun, Timothy Klouda, Suzanne Barnasconi, Ingrid Schalij et autres

We attempted to establish a mouse model of severe and irreversible pulmonary hypertension by substituting hypoxia with pulmonary overcirculation. To do so, we treated mice with either SU5416 or monocrotaline pyrrole after pneumonectomy and performed hemodynamic evaluations for PH. Despite this "two-hit" …

nl, us, dk, jp (code pays fourni par la source)

Imaging the TGFβ type I receptor in pulmonary arterial hypertension

Lonneke Rotteveel, Alex J. Poot, Esther Kooijman, Robert C. Schuit et autres

Abstract Transforming growth factor β (TGFβ) activity is perturbed in remodelled pulmonary vasculature of patients with pulmonary arterial hypertension (PAH), cancer, vascular diseases and developmental disorders. Inhibition of TGFβ, which signals via activin receptor-like kinase 5 (ALK5), prevents progression and development of …

nl (code pays fourni par la source)

Work and oxygen consumption of isolated right ventricular papillary muscle in experimental pulmonary hypertension

Willem J. van der Laarse, Sylvia J. P. Bogaards, Ingrid Schalij, Anton Vonk Noordegraaf et autres

Abstract Right‐sided myocardial mechanical efficiency (work output/metabolic energy input) in pulmonary hypertension can be severely reduced. We determined the contribution of intrinsic myocardial determinants of efficiency using papillary muscle preparations from monocrotaline‐induced pulmonary hypertensive (MCT‐PH) rats. The hypothesis tested was that efficiency …

nl (code pays fourni par la source)

Work and oxygen consumption of isolated right ventricular papillary muscle in experimental pulmonary hypertension

Willem J. van der Laarse, Sylvia J. P. Bogaards, Ingrid Schalij, Anton Vonk Noordegraaf et autres

Summary Right-sided myocardial mechanical efficiency (work output/metabolic energy input) in pulmonary hypertension can be severely reduced. We determined the contribution of intrinsic myocardial determinants of efficiency using papillary muscle preparations from monocrotaline-induced pulmonary hypertensive (MCT-PH) rats. The hypothesis was tested that efficiency …

nl (code pays fourni par la source)

Abstract 12771: HDAC Inhibition With Quisinostat Reduces Pulmonary Vascular Remodeling in Experimentally Induced Pulmonary Arterial Hypertension

Xiaoqing Sun, Quint A. J. Hagdorn, Diederik van der Feen, Eva L. Peters et autres

Introduction: Histone deacetylases (HDACs) expression and activity are increased in pulmonary arterial hypertension (PAH). Although inhibiting HDACs has been promoted as a treatment for PAH, results from preclinical studies were equivocal and raised concerns regarding safety. Quisinostat is a “second generation” HDAC …

nl (code pays fourni par la source)

Altered TGFβ/SMAD Signaling in Human and Rat Models of Pulmonary Hypertension: An Old Target Needs Attention

Takayuki Jujo, Xiao‐Qing Sun, Chris Happé, Christophe Guignabert et autres

Recent translational studies highlighted the inhibition of transforming growth factor (TGF)-β signaling as a promising target to treat pulmonary arterial hypertension (PAH). However, it remains unclear whether alterations in TGF-β signaling are consistent between PAH patients and animal models. Therefore, we compared …

nl, fr (code pays fourni par la source)

Increased MAO-A Activity Promotes Progression of Pulmonary Arterial Hypertension

Xiao‐Qing Sun, Eva L. Peters, Ingrid Schalij, Julie Birkmose Axelsen et autres

Monoamine oxidases (MAOs), a class of enzymes bound to the outer mitochondrial membrane, are important sources of reactive oxygen species. Increased MAO-A activity in endothelial cells and cardiomyocytes contributes to vascular dysfunction and progression of left heart failure. We hypothesized that inhibition …

dk, nl (code pays fourni par la source)

HDAC inhibitor quisinostat reduces pulmonary vascular remodeling in experimentally induced pulmonary arterial hypertension

Xiao‐Qing Sun, Eva L. Peters, Ingrid Schalij, Frances S. de Man et autres

Histone deacetylases (HDACs) are increased in pulmonary arterial hypertension (PAH), and inhibiting HDACs can be a promising treatment for PAH. However, previous studies on experimental PAH revealed controversial results, and adverse effects are common. Quisinostat is a “second generation” HDACs inhibitor, which …

nl (code pays fourni par la source)

The need for hypoxic exposure in experimental PAH - Comment on Chen et al.: a novel rat model of pulmonary hypertension induced by mono treatment with SU5416

Michiel Alexander de Raaf, Ingrid Schalij, Harm Jan Bogaard

nl (code pays fourni par la source)

MnTBAP Reverses Pulmonary Vascular Remodeling and Improves Cardiac Function in Experimentally Induced Pulmonary Arterial Hypertension

Maria Catalina Gomez‐Puerto, Xiao‐Qing Sun, Ingrid Schalij, Mar Orriols et autres

Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by obstructed pulmonary vasculatures. Current therapies for PAH are limited and only alleviate symptoms. Reduced levels of BMPR2 are associated with PAH pathophysiology. Moreover, reactive oxygen species, inflammation and autophagy have been shown …

nl, de (code pays fourni par la source)

The BMP Receptor 2 in Pulmonary Arterial Hypertension: When and Where the Animal Model Matches the Patient

Chris Happé, Kondababu Kurakula, Xiao‐Qing Sun, Denielli da Silva Gonçalves Bós et autres

Background: Mutations in bone morphogenetic protein receptor type II (BMPR2) are leading to the development of hereditary pulmonary arterial hypertension (PAH). In non-hereditary forms of PAH, perturbations in the transforming growth factor-β (TGF-β)/BMP-axis are believed to cause deficient BMPR2 signaling by changes …

nl, fr, es (code pays fourni par la source)

Inhibition of monoamine oxidase A in pulmonary artery banding-induced right ventricular failure

Eva L. Peters, Xiao‐Qing Sun, Stine Andersen, Julie Birkmose Axelsen et autres

nl, dk (code pays fourni par la source)