Marc Humbert works in Vascular / Pulmonary Vascular affiliated with Inserm.
Marc Humbert is Dean of the Faculty of Medicine and Professor of Respiratory Medicine at Université Paris-Saclay. He is Head of the Department of Pulmonology and Respiratory Intensive Care at Bicêtre Hospital (AP-HP), which hosts the French Pulmonary Hypertension Reference Centre, and Director of the Inserm/Université Paris-Saclay research unit on Pulmonary Hypertension: Pathophysiology and Therapeutic Innovation.
2,211 pubs · 154,821 cites · h-index 175
MD
Université Paris-Sud
1994
PhD (Immunology)
Université Paris-Sud
1993
Dean of the Faculty of Medicine and Professor of Respiratory Medicine
Université Paris-Saclay · 2023 - Present
Head of Department of Pulmonology and Respiratory Intensive Care / French Pulmonary Hypertension Reference Centre
Bicêtre Hospital, AP-HP · 2016 - Present
Director
Inserm UMR_S 1358 (HPPIT), Université Paris-Saclay · 2010 - Present
Professor of Respiratory Medicine
Université Paris-Sud / Université Paris-Saclay · 1999 - Present
Postdoctoral Fellow
Imperial College London · 1993 - 1995
JHLT OpenChemla et al.cross-sectional
In pulmonary hypertension, using a recalibrated 0.37 form factor or the geometric mean formula eliminates the systematic bias seen with the conventional 0.33 formula when estimating or reconstructing pulmonary arterial pressures.
European Respiratory JournalMontani et al.Original Research
Extract Pulmonary arterial hypertension (PAH) is characterized by distal pulmonary arteriolar remodelling with a progressive rise in pulmonary vascular resistance (PVR), right-ventricular (RV) dysfunction, and, in the absence of effective therapy, premature death [1]. Pathogenic variants in the BMPR2 gene, which encodes bone morphogenetic protein receptor type II (BMPR-II) represent the most common genetic predisposition to heritable PAH [2]. Beyond BMPR2, overactivation of the pro-proliferative TGF-#x03B2;–activin–nodal axis plays a pivotal role in driving obstructive vascular remodelling in PAH pathogenesis.
JACCPerros et al.Original Research
CirculationMontani et al.Original Research
Pulmonary hypertension specialist, Université Paris-Sud · Université Paris-Sud
These early dropouts make the interpretation of the positive results of the study debatable, because many patients did not reach the end of the 6-month trial. It is possible that the most severely affected patients were not able to tolerate the active treatment regimen, thus artificially enriching the long-term treated population with subjects characterized by a better phenotype.
CirculationHumbert
CirculationHumbert et al.Original Research
JACCSoubrier et al.review
This review highlights major genetic discoveries in pulmonary arterial hypertension, including BMPR2 mutations, and the role of next-generation sequencing in advancing diagnosis and understanding disease mechanisms.
Dialogues in sociology.HumbertOriginal Research
European Respiratory JournalGrynblat et al.Review
Narrative review uncovers complex etiologies of pulmonary hypertension across rare genetic syndromes, highlighting distinct developmental mechanisms and opportunities for precision management.
JACCManders et al.case-control
LV cardiomyocyte atrophy and weakness may contribute to PAH-related LV impairment; hypothesis-generating for targeted therapies, needs prospective validation.
European Respiratory JournalGuignabert et al.Original Research
Review demonstrates bimodal regulation of vascular tone in pulmonary disorders, suggesting therapeutic tuning rather than pathway activation is key.
European Respiratory JournalKovács et al.Guideline
Endorses sotatercept add-on for intermediate- to high-risk PAH on background therapy; extends RCT data into updated guideline-directed care.
Science Translational MedicineBikou et al.Original Research
Preclinical study reveals that microRNA-224 inhibition reverses vascular remodeling in animal models of pulmonary arterial hypertension, indicating a promising therapeutic target.
JHLT OpenPradère et al.Original Research
Background Despite major advances in targeted therapies, lung transplantation remains a key option for selected patients with end-stage pulmonary arterial hypertension (PAH) but is associated with substantial clinical and organizational challenges. Our aim was to describe the impact of changes in advanced PAH management and referral strategies on the profile of transplanted patients and outcomes. Methods All patients with PAH (except congenital heart disease), who underwent lung or heart–lung transplantation between 2008 and 2023 were retrospectively studied in France. Data were obtained from the National PAH and Transplant Registries. Patient characteristics, transplant strategies, and outcomes were compared between 2008–2015 (period 1) and 2016–2023 (period 2). Results Overall, 241 PAH patients underwent transplantation. The proportion of patients aged ≥50 years increased from 30% to 44% (p=0.04). Time from diagnosis to transplantation tended to increase (39 vs. 46 months, p=0.2). Pre-operative extracorporeal membrane oxygenation (ECMO) as a bridge to transplantation increased from 6% to 14% (p=0.05), while post-operative ECMO use remained stable (35% vs. 36%). Three-month post-transplant survival was 85% (95% CI 78–92%) and 91% (95% CI 86–96%) in periods 1 and 2, respectively. In the PAH population aged <65 years, the ratio of deaths without transplantation to transplantations performed exceeded 5:1, with marked heterogeneity across aetiologies. Conclusion Advances in severe PAH management have enabled transplantation in older and more intensively treated patients without compromising short-term outcomes. However, major disparities in access to transplantation persist across PAH aetiologies, underscoring the persistent challenges in advanced PAH management.
EHJPitre et al.editorial
This analysis evaluated treatments in 6,811 patients with pulmonary arterial hypertension across 20 trials. Combined therapy targeting the endothelin and nitric oxide pathways improved walking distance and delayed clinical worsening compared with alternatives. The catch: the review only included trials submitted to the FDA, likely excluding negative studies. Treatment effects varied by age, body mass index and comorbidities, introducing new hypotheses for personalizing therapy.
JACCHumbert et al.review
This review highlights the complex cellular and molecular mechanisms underlying pulmonary arterial hypertension, identifying key pathways that serve as current and potential pharmacological targets.
Vascular / Pulmonary Vascular · University of Michigan
Ralinepag reduced the risk of a first clinical worsening event and increased clinical improvement, maintaining durability of effect in this long-term clinical trial in PAH patients who were on dual background therapy. These findings support ralinepag as an oral, once-daily prostacyclin pathway treatment option upon FDA approval and suggest that the addition of prostacyclin pathway therapy can reduce clinical worsening even in a largely pretreated population with relatively preserved baseline functional capacity.
LancetMcLaughlin et al.RCT
ADVANCE OUTCOMES tested the daily pill ralinepag against a placebo in 687 pulmonary arterial hypertension patients. At roughly 80 weeks median follow up, 18% on ralinepag versus 36% on placebo died, had a hospital stay for worsening disease or right heart failure, started injected or inhaled therapy, progressed, or had an unsatisfactory response. The catch: side effects led 19% of treated patients to stop the drug versus 3% on placebo.
ERJ Open ResearchNeagu et al.cohort
Renal dysfunction was associated with worse PAH outcomes; leaves open whether adding eGFR to risk scores improves stratification or requires prospective validation.
EHJMembers et al.Guideline
Provides the 2014 European Society of Cardiology standard of care for diagnosing and managing acute pulmonary embolism.
CirculationHuertas et al.Original Research
