📇 Rhumatologue · LA ROCHELLE CEDEX 1 · (17) · Libéral

M Killian MARTIN

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3 raisons identifiées

Auteur de référence en rhumatologie
27 articles scientifiques publiés — un praticien à la pointe de la recherche
Disponibilité géographique
2 lieux d'exercice — choisissez celui qui vous arrange
Délais de RDV courts dans la région
120.2 rhumatos / 100 000 hab. — département bien doté

Rhumatologue

📍 LA ROCHELLE CEDEX 1 (17)LibéralRPPS 10101618659

4ans d'exercice (thèse 2022)

📊 Reconnaissance scientifique : 15/100📝 69 articles publiés🇫🇷 Publications académiques françaises (7)

✨ Génération du profil synthétique IA en cours…

Thèses universitaires

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

Reduced Platelet miR-223 Induction in Kawasaki Disease Leads to Severe Coronary Artery Pathology Through a miR-223/PDGFRβ Vascular Smooth Muscle Cell Axis

Circulation research · 2020

📚 60 citations🎯 RCR 3.28Top 14% NIH🔓 Open Access

Lire l'abstract Crossref ↓

Rationale: Kawasaki disease (KD) is an acute vasculitis of early childhood that can result in permanent coronary artery structural damage. The cause for this arterial vulnerability in up to 15% of patients with KD is unknown. Vascular smooth muscle cell dedifferentiation play a key role in the pathophysiology of medial damage and aneurysm formation, recognized arterial pathology in KD. Platelet hyperreactivity is also a hallmark of KD. We recently demonstrated that uptake of platelets and platelet-derived miRNAs influences vascular smooth muscle cell phenotype in vivo. Objective: We set out to explore whether platelet/vascular smooth muscle cell (VSMC) interactions contribute to coronary pathology in KD. Methods and Results: We prospectively recruited and studied 242 patients with KD, 75 of whom had documented coronary artery pathology. Genome-wide miRNA sequencing and droplet digital PCR demonstrated that patient with KD platelets have significant induction of miR-223 compared with healthy controls (HCs). Platelet-derived miR-223 has recently been shown to promote vascular smooth muscle quiescence and resolution of wound healing after vessel injury. Paradoxically, patients with KD with the most severe coronary pathology (giant coronary artery aneurysms) exhibited a lack of miR-223 induction. Hyperactive platelets isolated from patients with KD are readily taken up by VSMCs, delivering functional miR-223 into the VSMCs promoting VSMC differentiation via downregulation of PDGFRβ (platelet-derived growth factor receptor β). The lack of miR-223 induction in patients with severe coronary pathology leads to persistent VSMC dedifferentiation. In a mouse model of KD ( Lactobacillus casei cell wall extract injection), miR-223 knockout mice exhibited increased medial thickening, loss of contractile VSMCs in the media, and fragmentation of medial elastic fibers compared with WT mice, which demonstrated significant miR-223 induction upon Lactobacillus casei cell wall extract challenge. The excessive arterial damage in the miR-223 knockout could be rescued by adoptive transfer of platelet, administration of miR-223 mimics, or the PDGFRβ inhibitor imatinib mesylate. Interestingly, miR-223 levels progressively increase with age, with the lowest levels found in <5-year-old. This provides a basis for coronary pathology susceptibility in this very young cohort. Conclusions: Platelet-derived miR-223 (through PDGFRβ inhibition) promotes VSMC differentiation and resolution of KD induced vascular injury. Lack of miR-223 induction leads to severe coronary pathology characterized by VSMC dedifferentiation and medial damage. Detection of platelet-derived miR-223 in patients with KD (at the time of diagnosis) may identify patients at greatest risk of coronary artery pathology. Moreover, targeting platelet miR-223 or VSMC PDGFRβ represents potential therapeutic strategies to alleviate coronary pathology in KD. Graphic Abstract: A graphic abstract is available for this article.

Fc receptors gone wrong: A comprehensive review of their roles in autoimmune and inflammatory diseases

Autoimmunity reviews · 2022

📚 38 citations🎯 RCR 3.27Top 14% NIH🔓 Open Access📄 PDF gratuit ↗

Bone Disease in Chronic Kidney Disease and Kidney Transplant

Nutrients · 2022

📚 30 citations🎯 RCR 3.71Top 12% NIH🔓 Open Access📄 PDF gratuit ↗

Lire l'abstract Crossref ↓

Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) comprises alterations in calcium, phosphorus, parathyroid hormone (PTH), Vitamin D, and fibroblast growth factor-23 (FGF-23) metabolism, abnormalities in bone turnover, mineralization, volume, linear growth or strength, and vascular calcification leading to an increase in bone fractures and vascular disease, which ultimately result in high morbidity and mortality. The bone component of CKD-MBD, referred to as renal osteodystrophy, starts early during the course of CKD as a result of the effects of progressive reduction in kidney function which modify the tight interaction between mineral, hormonal, and other biochemical mediators of cell function that ultimately lead to bone disease. In addition, other factors, such as osteoporosis not apparently dependent on the typical pathophysiologic abnormalities resulting from altered kidney function, may accompany the different varieties of renal osteodystrophy leading to an increment in the risk of bone fracture. After kidney transplantation, these bone alterations and others directly associated or not with changes in kidney function may persist, progress or transform into a different entity due to new pathogenetic mechanisms. With time, these alterations may improve or worsen depending to a large extent on the restoration of kidney function and correction of the metabolic abnormalities developed during the course of CKD. In this paper, we review the bone lesions that occur during both CKD progression and after kidney transplant and analyze the factors involved in their pathogenesis as a means to raise awareness of their complexity and interrelationship.

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M Killian MARTIN

Pourquoi vous devez consulter ce praticien

Thèses universitaires

Activité de recherche & publications

Publications académiques en France

Lieux de consultation(2)

Tarifs & secteur de conventionnement

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Top publications · les plus citées

Publications scientifiques (27) — classées par pathologie

Transversal12

Revue générale3

Santé mentale / fatigue2

Sjögren2

Activité physique / Rééducation1

Anti-TNF1

Case report / série1

Épidémiologie & registres1

Essai clinique1

Lupus1

Microbiote1

Revue / méta-analyse1

SAPL1

Tendinopathies & SCC1

Vraie vie / RWE1

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