Steeve Provencher

ORCID: 0000-0001-7535-9972
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About
Contact & Profiles
Research Areas
  • Pulmonary Hypertension Research and Treatments
  • Cardiovascular Function and Risk Factors
  • RNA modifications and cancer
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • MicroRNA in disease regulation
  • Circular RNAs in diseases
  • Respiratory Support and Mechanisms
  • Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
  • Venous Thromboembolism Diagnosis and Management
  • Peptidase Inhibition and Analysis
  • Cancer-related molecular mechanisms research
  • Cardiovascular Issues in Pregnancy
  • Cardiovascular and exercise physiology
  • Vascular Anomalies and Treatments
  • Heart Failure Treatment and Management
  • Protein Degradation and Inhibitors
  • Atrial Fibrillation Management and Outcomes
  • Cardiovascular Effects of Exercise
  • Medical Imaging and Pathology Studies
  • ATP Synthase and ATPases Research
  • COVID-19 Clinical Research Studies
  • Mitochondrial Function and Pathology
  • Cardiac Valve Diseases and Treatments
  • Congenital Heart Disease Studies
  • Cardiovascular Disease and Adiposity

Institut Universitaire de Cardiologie et de Pneumologie de Québec
2016-2025

Université Laval
2016-2025

Lung Institute
2025

Montreal Heart Institute
2008-2024

Quebec - Clinical Research Organization in Cancer
2020-2024

Pulmonary Hypertension Association
2017-2024

Canadian Heart Research Centre
2021-2024

Pulmonary Associates
2023

Isabela State University
2023

Université du Québec
2021

Characteristics of patients with idiopathic pulmonary arterial hypertension (IPAH) who benefit from long-term calcium channel blockers (CCB) are unknown.Acute vasodilator testing epoprostenol or nitric oxide was performed in 557 IPAH patients. Acute responders, defined by a fall both mean artery pressure (PAP) and vascular resistance (PVR) >20%, received oral CCB. Patients CCB were as those being New York Heart Association (NYHA) functional class I II after at least 1 year on monotherapy....

10.1161/circulationaha.104.488486 article EN Circulation 2005-06-07

Pulmonary arterial hypertension (PAH) is characterized by enhanced proliferation and reduced apoptosis of pulmonary artery smooth muscle cells (PASMCs). Because microRNAs have been recently implicated in the regulation cell apoptosis, we hypothesized that these regulatory molecules might be etiology PAH. In this study, show miR-204 expression PASMCs down-regulated both human rodent down-regulation correlates with PAH severity accounts for proliferative antiapoptotic phenotypes PAH-PASMCs....

10.1084/jem.20101812 article EN The Journal of Experimental Medicine 2011-02-14

Pulmonary arterial hypertension (PAH) is associated with sustained inflammation known to promote DNA damage. Despite these unfavorable environmental conditions, PAH pulmonary smooth muscle cells (PASMCs) exhibit, in contrast healthy PASMCs, a pro-proliferative and anti-apoptotic phenotype, time by the activation of miR-204, nuclear factor activated T cells, hypoxia-inducible 1-α. We hypothesized that PAH-PASMCs have increased poly(ADP-ribose) polymerase-1 (PARP-1), critical enzyme implicated...

10.1161/circulationaha.113.006167 article EN Circulation 2013-11-23

Right ventricular (RV) failure is the most important factor of both morbidity and mortality in pulmonary arterial hypertension (PAH). However, underlying mechanisms resulting failed RV PAH remain unknown. There growing evidence that angiogenesis microRNAs are involved PAH-associated failure. We hypothesized microRNA-126 (miR-126) downregulation decreases microvessel density promotes transition from a compensated to decompensated PAH.We studied free wall tissues humans with normal (n=17),...

10.1161/circulationaha.115.016382 article EN Circulation 2015-07-11

Pulmonary arterial hypertension (PAH) remains a mysterious killer that, like cancer, is characterized by tremendous complexity. PAH development occurs under sustained and persistent environmental stress, such as inflammation, shear pseudo-hypoxia, more. After inducing an initial death of the endothelial cells, these stresses contribute with time to hyper-proliferative apoptotic resistant clone cells including pulmonary artery smooth muscle fibroblasts, even allowing vascular remodeling...

10.1177/2045893217701438 article EN cc-by-nc Pulmonary Circulation 2017-03-01

Rationale: Pulmonary arterial hypertension (PAH) often results in death from right ventricular failure (RVF). NLRP3 (nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3)-macrophage activation may promote RVF PAH. Objectives: Evaluating the contribution of inflammasome RV macrophages to PAH RVF. Methods: Rats with decompensated hypertrophy (monocrotaline [MCT] and Sugen-5416 hypoxia [SuHx]) were compared compensated rats (pulmonary artery banding)....

10.1164/rccm.202110-2274oc article EN American Journal of Respiratory and Critical Care Medicine 2022-06-14

Aims Data on long-term efficacy of bosentan in unselected idiopathic pulmonary arterial hypertension (IPAH) patients are lacking. We aimed to describe the outcome consecutive IPAH treated first-line with bosentan.

10.1093/eurheartj/ehi728 article EN European Heart Journal 2006-01-23

This large, prospective, multicentric study was performed to analyze the distribution of tricuspid regurgitation velocity (TRV) values during exercise and hypoxia in relatives patients with idiopathic familial pulmonary arterial hypertension (PAH) healthy control subjects. We tested hypothesis that idiopathic/familial PAH display an enhanced frequency hypertensive TRV response stress this is associated mutations bone morphogenetic protein receptor II (BMPR2) gene.TRV estimated by Doppler...

10.1161/circulationaha.108.800938 article EN Circulation 2009-03-24

<h3>Background</h3> A majority of patients with idiopathic pulmonary arterial hypertension (IPAH) display persistent exercise intolerance despite new specific therapies. Whether IPAH exhibit peripheral muscle dysfunction that may contribute to this limitation remains unknown. The hypothesis the muscles are weaker and morphological changes compared those control subjects partly correlate their capacity was tested. <h3>Objective</h3> To characterise quadriceps function, morphology enzymatic...

10.1136/thx.2009.117168 article EN Thorax 2009-08-30

Pulmonary artery hypertension (PAH) is a proliferative disorder associated with enhanced pulmonary smooth muscle cell proliferation and suppressed apoptosis. The sustainability of this phenotype required the activation prosurvival transcription factor like signal transducers activators transcription-3 (STAT3) nuclear activated T (NFAT). Because these factors are implicated in several physiological processes, their inhibition PAH patients could be detrimental effects. Therefore, better...

10.1161/circulationaha.110.963314 article EN Circulation 2011-03-08

Rationale: Pulmonary arterial hypertension (PAH) is a vasculopathy characterized by enhanced pulmonary artery (PA) smooth muscle cell (PASMC) proliferation and suppressed apoptosis. Decreased expression of microRNA-204 has been associated to this phenotype. By still elusive mechanism, downregulation promotes the oncogenes, including nuclear factor activated T cells, B-cell lymphoma 2, Survivin. In cancer, increased epigenetic reader bromodomain-containing protein 4 (BRD4) sustains survival...

10.1161/circresaha.115.307004 article EN Circulation Research 2015-07-30

Rationale: Lower limb muscle dysfunction contributes to exercise intolerance in chronic obstructive pulmonary disease (COPD). We hypothesized that signaling from lower group III/IV sensory afferents the central motor command could be involved premature cycling termination COPD.Objectives: To evaluate effects of spinal anesthesia, which presumably inhibited feedback on tolerance and cardiorespiratory response during constant work-rate patients with COPD.Methods: In a crossover double-blind...

10.1164/rccm.201203-0404oc article EN American Journal of Respiratory and Critical Care Medicine 2012-07-21

Rationale: Pulmonary arterial hypertension (PAH) is an obstructive vasculopathy characterized by excessive pulmonary artery smooth muscle cell (PASMC) proliferation, migration, and apoptosis resistance. This cancer-like phenotype promoted increased cytosolic calcium ([Ca2+]cyto), aerobic glycolysis, mitochondrial fission.Objectives: To determine how changes in uniporter (MCU) complex (MCUC) function influence dynamics contribute to PAH’s phenotype.Methods: PASMCs were isolated from patients...

10.1164/rccm.201604-0814oc article EN American Journal of Respiratory and Critical Care Medicine 2016-09-20

Right ventricular (RV) function is the major determinant for both functional capacity and survival in patients with pulmonary arterial hypertension (PAH). Despite recognized clinical importance of preserving RV function, subcellular mechanisms that govern transition from a compensated to decompensated state remain poorly understood as consequence there are no clinically established treatments failure paucity useful biomarkers. Accumulating evidence indicates long noncoding RNAs powerful...

10.1161/circulationaha.120.047626 article EN Circulation 2020-07-23
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