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Véronique Capuano
French Institute of Health and Medical Research
EndocrinologyCardiologyMyocytePulmonary hypertensionBiology
9Publications
4H-index
104Citations
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Publications 9
Newest
#1Mélanie Lambert (French Institute of Health and Medical Research)H-Index: 4
#2Véronique Capuano (French Institute of Health and Medical Research)H-Index: 4
Last. Fabrice Antigny (French Institute of Health and Medical Research)H-Index: 21
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Rationale: Pulmonary arterial hypertension is a severe lethal cardiopulmonary disease. Loss of function mutations in KCNK3 (potassium channel subfamily K member 3) gene, which encodes an outward re...
3 CitationsSource
#1Jennifer Arthur Ataam (Stanford University)H-Index: 3
#2Olaf Mercier (French Institute of Health and Medical Research)H-Index: 11
Last. Saadia Eddahibi (University of Montpellier)H-Index: 50
view all 13 authors...
BACKGROUND Pulmonary endothelial cells play a key role in the pathogenesis of Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Increased synthesis and/or the release of intercellular adhesion molecule-1 (ICAM-1) by pulmonary endothelial cells of patients with CTEPH has been recently reported, suggesting a potential role for ICAM-1 in CTEPH. METHODS We studied pulmonary endarterectomy specimens from 172 patients with CTEPH and pulmonary artery specimens from 97 controls undergoing lobectomy...
1 CitationsSource
Pulmonary arterial hypertension (PAH) is a multifactorial and severe disease without curative therapies. PAH pathobiology involves altered pulmonary arterial tone, endothelial dysfunction, distal pulmonary vessel remodeling, and inflammation, which could all depend on ion channel activities (K+, Ca2+, Na+ and Cl−). This review focuses on ion channels in the pulmonary vasculature and discusses their pathophysiological contribution to PAH as well as their therapeutic potential in PAH.
8 CitationsSource
Source
#1Mélanie Lambert (French Institute of Health and Medical Research)H-Index: 4
#2Angèle BoetH-Index: 2
Last. Fabrice Antigny (French Institute of Health and Medical Research)H-Index: 21
view all 19 authors...
10 CitationsSource
#1Safietou Sankhe (French Institute of Health and Medical Research)H-Index: 1
#2Sevasti Manousakidi (French Institute of Health and Medical Research)H-Index: 1
Last. Véronique Capuano (French Institute of Health and Medical Research)H-Index: 4
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Abstract Idiopathic pulmonary arterial hypertension (iPAH) is characterized by obstructive hyperproliferation and apoptosis resistance of distal pulmonary artery smooth muscle cells (PASMCs). T-type Ca 2 + channel blockers have been shown to reduce experimental pulmonary hypertension, although the impact of T-type channel inhibition remains unexplored in PASMCs from iPAH patients. Here we show that T-type channels Cav3.1 and Cav3.2 are present in the lung and PASMCs from iPAH patients and contro...
4 CitationsSource
#1Yann RuchonH-Index: 3
#2Laurent FerronH-Index: 12
Last. Véronique CapuanoH-Index: 4
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Recent studies indicate that cardiac T-type Ca2+ current (ICaT) reappears in hypertrophied ventricular cells. The aim of this study was to investigate the role of angiotensin II (Ang II), a major inducer of cardiac hypertrophy, in the reexpression of T-type channel in left ventricular hypertrophied myocytes. We induced cardiac hypertrophy in rats by abdominal aorta stenosis for 12 weeks and thereafter animals were treated for 2 weeks with losartan (12 mg/kg per day), an antagonist of type 1 Ang ...
#1Laurent FerronH-Index: 12
#2Véronique CapuanoH-Index: 4
Last. Jean-François RenaudH-Index: 12
view all 6 authors...
Recent studies indicate that cardiac T-type Ca 2+ current ( I CaT ) reappears in hypertrophied ventricular cells. The aim of this study was to investigate the role of angiotensin II (Ang II), a major inducer of cardiac hypertrophy, in the reexpression of T-type channel in left ventricular hypertrophied myocytes. We induced cardiac hypertrophy in rats by abdominal aorta stenosis for 12 weeks and thereafter animals were treated for 2 weeks with losartan (12 mg/kg per day), an antagonist of type 1 ...
82 CitationsSource
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