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📇 Rhumatologue · Montpellier · (34) · Hospitalier

Docteur CEDRIC LUKAS

Pourquoi vous devez consulter ce praticien

3 raisons identifiées

  • Plateau technique de référence

    Centre hospitalier universitaire (CHU) — équipements et expertise pointus pour les cas complexes

  • Auteur de référence en rhumatologie

    50 articles scientifiques publiés — un praticien à la pointe de la recherche

  • Référence presse grand public

    Cité 1 fois dans les médias — pédagogie reconnue

Rhumatologue
📍 Montpellier (34)HospitalierRPPS 10005165096
📊 Reconnaissance scientifique : 33/100📝 223 articles publiés🇫🇷 Publications académiques françaises (8)

✨ Profil synthétique

IA · 30/04/2026

Le Docteur CEDRIC LUKAS est un rhumatologue hospitalier à Montpellier, avec une activité de recherche significative dans le domaine des maladies auto-immunes et inflammatoires. Ses travaux de recherche portent notamment sur la polyarthrite rhumatoïde, la spondylarthrite et le lupus érythémateux systémique. Avec un h-index de 33 et plus de 223 publications, il démontre une expertise reconnue dans ces domaines.

Expertises présumées

  • Rheumatoid Arthritis
  • Spondyloarthritis
  • Systemic Lupus Erythematosus
  • Psoriasis
  • Biothérapies non-anti-TNF
  • Thérapies anti-IL-17
  • csDMARDs

Synthèse automatique à partir des sources publiques (HAL, OpenAlex, theses.fr, ClinicalTrials.gov, FAI²R, ANS). Pas une évaluation clinique. Le médecin peut corriger via son compte.

Diplômes

🎓 DES & spécialité ordinale

  • DES Rhumatologie
  • Rhumatologie (SM)

🎓 Diplômes

  • DE Docteur en médecine

Source : Annuaire Santé ANS (FHIR Practitioner.qualification) · Mises à jour quotidiennes.

Activité de recherche & publications

Indicateurs publics agrégés sur 250 M+ d'œuvres scientifiques (OpenAlex, PubMed). Traduits ici en langage patient.

Influence scientifique

33

33 articles ont été cités au moins 33fois par d'autres chercheurs — preuve que ses travaux sont repris par la communauté médicale.

h-index

Total citations reçues

4 870

Nombre de fois où d'autres équipes ont mentionné ses publications dans leurs propres travaux.

Publications totales

223

Articles, revues et chapitres référencés dans les bases académiques internationales.

Articles influents

64

Publications ayant marqué leur domaine — chacune citée au moins 10 fois par d'autres chercheurs.

i10-index

Thématiques principales

  • Rheumatoid Arthritis Research and Therapies ×147
  • Spondyloarthritis Studies and Treatments ×107
  • Autoimmune and Inflammatory Disorders Research ×31
  • Systemic Lupus Erythematosus Research ×29
  • Psoriasis: Treatment and Pathogenesis ×24

Affiliations FR : Centre National de la Recherche Scientifique · Inserm · Université de Montpellier

Source : OpenAlex (CC0, OurResearch). Indicateurs académiques agrégés sur 250 M+ d'œuvres.

Publications académiques en France

Articles déposés en accès libre sur l'archive ouverte des universités françaises (HAL) — gage d'activité de recherche en France.

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

Lieu de consultation

Plan généré via la Base Adresse Nationale (api-adresse.data.gouv.fr). Précision indicative.

Tarifs & secteur de conventionnement

Secteur de conventionnement non disponible (médecin hospitalier ou non présent dans l'Annuaire santé CNAM des libéraux conventionnés).

Prendre rendez-vous & contact

Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).

Articles de presse (1)

Source : Google News (recherche par nom complet — homonymes possibles, vérifier le contenu).

Top publications · les plus citées

  • 1
    Curcumin-primed human BMSC-derived extracellular vesicles reverse IL-1β-induced catabolic responses of OA chondrocytes by upregulating miR-126-3p

    Stem cell research & therapy · 2021

    📚 75 citations🎯 RCR 5.85Top 6% NIH🔓 Open Access📄 PDF gratuit ↗
    Lire l'abstract Crossref ↓

    AbstractBackgroundCurcumin has anti-inflammatory effects and qualifies as a potential candidate for the treatment of osteoarthritis (OA). However, curcumin has limited bioavailability. Extracellular vesicles (EVs) are released by multiple cell types and act as molecule carrier during intercellular communication. We assume that EVs can maintain bioavailability and stability of curcumin after encapsulation. Here, we evaluated modulatory effects of curcumin-primed human (h)BMSC-derived EVs (Cur-EVs) on IL-1β stimulated human osteoarthritic chondrocytes (OA-CH).MethodsCellTiter-Blue Viability- (CTB), Caspase 3/7-, and live/dead assays were used to determine range of cytotoxic curcumin concentrations for hBMSC and OA-CH. Cur-EVs and control EVs were harvested from cell culture supernatants of hBMSC by ultracentrifugation. Western blotting (WB), transmission electron microscopy, and nanoparticle tracking analysis were performed to characterize the EVs. The intracellular incorporation of EVs derived from PHK26 labeled and curcumin-primed or control hBMSC was tested by adding the labeled EVs to OA-CH cultures. OA-CH were pre-stimulated with IL-1β, followed by Cur-EV and control EV treatment for 24 h and subsequent analysis of viability, apoptosis, and migration (scratch assay). Relative expression of selected anabolic and catabolic genes was assessed with qRT-PCR. Furthermore, WB was performed to evaluate phosphorylation of Erk1/2, PI3K/Akt, and p38MAPK in OA-CH. The effect of hsa-miR-126-3p expression on IL-1β-induced OA-CH was determined using CTB-, Caspase 3/7-, live/dead assays, and WB.ResultsCur-EVs promoted viability and reduced apoptosis of IL-1β-stimulated OA-CH and attenuated IL-1β-induced inhibition of migration. Furthermore, Cur-EVs increased gene expression of BCL2, ACAN, SOX9, and COL2A1 and decreased gene expression of IL1B, IL6, MMP13, and COL10A1 in IL-1β-stimulated OA-CH. In addition, phosphorylation of Erk1/2, PI3K/Akt, and p38 MAPK, induced by IL-1β, is prevented by Cur-EVs. Cur-EVs increased IL-1β-reduced expression of hsa-miR-126-3p and hsa-miR-126-3p mimic reversed the effects of IL-1β.ConclusionCur-EVs alleviated IL-1β-induced catabolic effects on OA-CH by promoting viability and migration, reducing apoptosis and phosphorylation of Erk1/2, PI3K/Akt, and p38 MAPK thereby modulating pro-inflammatory signaling pathways. Treatment of OA-CH with Cur-EVs is followed by upregulation of expression of hsa-miR-126-3p which is involved in modulation of anabolic response of OA-CH. EVs may be considered as promising drug delivery vehicles of curcumin helping to alleviate OA.

  • 2
    hBMSC-Derived Extracellular Vesicles Attenuate IL-1β-Induced Catabolic Effects on OA-Chondrocytes by Regulating Pro-inflammatory Signaling Pathways

    Frontiers in bioengineering and biotechnology · 2020

    📚 50 citations🎯 RCR 3.13Top 15% NIH🔓 Open Access
    Lire l'abstract Crossref ↓

    Background: Human bone marrow-derived mesenchymal stromal cells (hBMSCs) provide a promising therapeutic approach in the cell-based therapy of osteoarthritis (OA). However, several disadvantages evolved recently, including immune responses of the host and regulatory hurdles, making it necessary to search for alternative treatment options. Extracellular vesicles (EVs) are released by multiple cell types and tissues into the extracellular microenvironment, acting as message carriers during intercellular communication. Here, we investigate putative protective effects of hBMSC-derived EVs as a cell-free approach, on IL-1β-stimulated chondrocytes obtained from OA-patients.Methods: EVs were harvested from the cell culture supernatant of hBMSCs by a sequential ultracentrifugation process. Western blot, scanning electron microscopy (SEM), and nanoparticle tracking analysis (NTA) were performed to characterize the purified particles as EVs. Intracellular incorporation of EVs, derived from PHK26-labeled hBMSCs, was tested by adding the labeled EVs to human OA chondrocytes (OA-CH), followed by fluorescence microscopy. Chondrocytes were pre-stimulated with IL-1β for 24 h, followed by EVs treatment for 24 h. Subsequently, proliferation, apoptosis, and migration (wound healing) were analyzed via BrdU assay, caspase 3/7 assay, and scratch assay, respectively. With qRT-PCR, the relative expression level of anabolic and catabolic genes was determined. Furthermore, immunofluorescence microscopy and western blot were performed to evaluate the protein expression and phosphorylation levels of Erk1/2, PI3K/Akt, p38, TAK1, and NF-κB as components of pro-inflammatory signaling pathways in OA-CH.Results: EVs from hBMSCs (hBMSC-EVs) promote proliferation and reduce apoptosis of OA-CH and IL-1β-stimulated OA-CH. Moreover, hBMSC-EVs attenuate IL-1β-induced reduction of chondrocyte migration. Furthermore, hBMSC-EVs increase gene expression of PRG4, BCL2, and ACAN (aggrecan) and decrease gene expression of MMP13, ALPL, and IL1ß in OA-CH. Notably, COL2A1, SOX9, BCL2, ACAN, and COMP gene expression levels were significantly increased in IL-1β+ EV groups compared with those IL-1β groups without EVs, whereas the gene expression levels of COLX, IL1B, MMP13, and ALPL were significantly decreased in IL-1β+ EV groups compared to IL-1β groups without EVs. In addition, the phosphorylation status of Erk1/2, PI3K/Akt, p38, TAK1, and NF-κB signaling molecules, induced by IL-1β, is prevented by hBMSC- EVs.Conclusion: EVs derived from hBMSCs alleviated IL-1β-induced catabolic effects on OA-CH via promoting proliferation and migration and reducing apoptosis, probably via downregulation of IL-1ß-activated pro-inflammatory Erk1/2, PI3K/Akt, p38, TAK1, and NF-κB signaling pathways. EVs released from BMSCs may be considered as promising cell-free intervention strategy in cartilage regenerative medicine, avoiding several adverse effects of cell-based regenerative approaches.

Publications scientifiques (50) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

Transversal20

Biothérapies non-anti-TNF6

Anti-IL-175

Épidémiologie & registres3

Revue / méta-analyse3

csDMARDs2

Revue générale2

Santé mentale / fatigue2

Sjögren2

AINS1

Anti-TNF1

Case report / série1

Échographie1

IA en rhumatologie1

JAK inhibiteurs1

Pharmacovigilance1

Recommandations1

Spondyloarthrite1

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