📇 Rhumatologue · TOURS CEDEX 9 · (37) · Hospitalier

M LAURENT PLANTIER

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4 raisons identifiées

Auteur de référence en rhumatologie
50 articles scientifiques publiés — un praticien à la pointe de la recherche
Encadrant universitaire
Forme la prochaine génération de rhumatologues (1 thèse dirigée)
Expérience confirmée
18 ans d'exercice en rhumatologie — recul clinique solide
Délais de RDV courts dans la région
131.9 rhumatos / 100 000 hab. — département bien doté

Rhumatologue

📍 TOURS CEDEX 9 (37)HospitalierRPPS 10001603280

Expérience confirmée

18ans d'exercice (thèse 2008)

📊 Reconnaissance scientifique : 27/100📝 199 articles publiés🇫🇷 Publications académiques françaises (8)🎓 1 thèse dirigée

✨ Génération du profil synthétique IA en cours…

Données ANS publiques (Licence Ouverte 2.0) · Enrichissements MonRhumato 100 % opt-in · Toute personne référencée peut demander la suppression ou la rectification.

Top publications · les plus citées

Physiology of the lung in idiopathic pulmonary fibrosis

European respiratory review : an official journal of the European Respiratory Society · 2018

📚 202 citations🎯 RCR 9.82Top 3% NIH🔓 Open Access📄 PDF gratuit ↗

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The clinical expression of idiopathic pulmonary fibrosis (IPF) is directly related to multiple alterations in lung function. These alterations derive from a complex disease process affecting all compartments of the lower respiratory system, from the conducting airways to the lung vasculature. In this article we review the profound alterations in lung mechanics (reduced lung compliance and lung volumes), pulmonary gas exchange (reduced diffusing capacity, increased dead space ventilation, chronic arterial hypoxaemia) and airway physiology (increased cough reflex and increased airway volume), as well as pulmonary haemodynamics related to IPF. The relative contribution of these alterations to exertional limitation and dyspnoea in IPF is discussed.

Rituximab and mycophenolate mofetil combination in patients with interstitial lung disease (EVER-ILD): a double-blind, randomised, placebo-controlled trial

The European respiratory journal · 2023

📚 99 citations🎯 RCR 15.23Top 1% NIH🩺 Clinique🔓 Open Access📄 PDF gratuit ↗

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BackgroundStandard of care for interstitial lung disease (ILD) with a nonspecific interstitial pneumonia (NSIP) pattern proposes mycophenolate mofetil (MMF) as one of the first-step therapies while rituximab is used as rescue therapy.MethodsIn a randomised, double-blind, two-parallel group, placebo-controlled trial (NCT02990286), patients with connective tissue disease-associated ILD or idiopathic interstitial pneumonia (with or without autoimmune features) and a NSIP pattern (defined on NSIP pathological pattern or on integration of clinicobiological data and a NSIP-like high-resolution computed tomography pattern) were randomly assigned in a 1:1 ratio to receive rituximab (1000 mg) or placebo on day 1 and day 15 in addition to MMF (2 g daily) for 6 months. The primary end-point was the change in percent predicted forced vital capacity (FVC) from baseline to 6 months analysed by a linear mixed model for repeated measures analysis. Secondary end-points included progression-free survival (PFS) up to 6 months and safety.FindingsBetween January 2017 and January 2019, 122 randomised patients received at least one dose of rituximab (n=63) or placebo (n=59). The least-squares mean change from baseline to 6 months in FVC (% predicted) was +1.60 (se1.13) in the rituximab+MMF group and −2.01 (se1.17) in the placebo+MMF group (between-group difference 3.60, 95% CI 0.41–6.80; p=0.0273). PFS was better in the rituximab+MMF group (crude hazard ratio 0.47, 95% CI 0.23–0.96; p=0.03). Serious adverse events occurred in 26 (41%) patients of the rituximab+MMF group and in 23 (39%) of the placebo+MMF group. Nine infections were reported in the rituximab+MMF group (five bacterial infections, three viral infections, one other) and four bacterial infections in the placebo+MMF group.InterpretationCombination of rituximab and MMF was superior to MMF alone in patients with ILD and a NSIP pattern. The use of this combination must take into consideration the risk of viral infection.

The Long Noncoding RNA DNM3OS Is a Reservoir of FibromiRs with Major Functions in Lung Fibroblast Response to TGF-β and Pulmonary Fibrosis

American journal of respiratory and critical care medicine · 2019

📚 98 citations🎯 RCR 4.05Top 11% NIH

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Abstract Rationale Given the paucity of effective treatments for idiopathic pulmonary fibrosis (IPF), new insights into the deleterious mechanisms controlling lung fibroblast activation, the key cell type driving the fibrogenic process, are essential to develop new therapeutic strategies. TGF-β (transforming growth factor-β) is the main profibrotic factor, but its inhibition is associated with severe side effects because of its pleiotropic role. Objectives To determine if downstream noncoding effectors of TGF-β in fibroblasts may represent new effective therapeutic targets whose modulation may be well tolerated. Methods We investigated the whole noncoding fraction of TGF-β–stimulated lung fibroblast transcriptome to identify new genomic determinants of lung fibroblast differentiation into myofibroblasts. Differential expression of the long noncoding RNA (lncRNA) DNM3OS (dynamin 3 opposite strand) and its associated microRNAs (miRNAs) was validated in a murine model of pulmonary fibrosis and in IPF tissue samples. Distinct and complementary antisense oligonucleotide–based strategies aiming at interfering with DNM3OS were used to elucidate the role of DNM3OS and its associated miRNAs in IPF pathogenesis. Measurements and Main Results We identified DNM3OS as a fibroblast-specific critical downstream effector of TGF-β–induced lung myofibroblast activation. Mechanistically, DNM3OS regulates this process in trans by giving rise to three distinct profibrotic mature miRNAs (i.e., miR-199a-5p/3p and miR-214-3p), which influence SMAD and non-SMAD components of TGF-β signaling in a multifaceted way. In vivo, we showed that interfering with DNM3OS function not only prevents lung fibrosis but also improves established pulmonary fibrosis. Conclusions Pharmacological approaches aiming at interfering with the lncRNA DNM3OS may represent new effective therapeutic strategies in IPF.

Cookies & analyse de trafic

M LAURENT PLANTIER

Pourquoi vous devez consulter ce praticien

Thèses universitaires

Direction de thèses

Activité de recherche & publications

Publications académiques en France

Lieu de consultation

Tarifs & secteur de conventionnement

Prendre rendez-vous & contact

Top publications · les plus citées

Publications scientifiques (50) — classées par pathologie

Transversal33

Essai clinique5

Biothérapies non-anti-TNF3

Épidémiologie & registres2

Revue générale2

csDMARDs1

Pédiatrie1

Recommandations1

Revue / méta-analyse1

Risque cardio-vasculaire1

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