A5023511215- DNA Repair Mechanisms
- Mitochondrial Function and Pathology
- Air Quality and Health Impacts
- Intensive Care Unit Cognitive Disorders
- Genetics and Neurodevelopmental Disorders
- Epigenetics and DNA Methylation
- Mesenchymal stem cell research
- Vehicle emissions and performance
- Polyamine Metabolism and Applications
- ATP Synthase and ATPases Research
- Nutrition and Health in Aging
- Muscle Physiology and Disorders
- Coenzyme Q10 studies and effects
- Air Quality Monitoring and Forecasting
- Telomeres, Telomerase, and Senescence
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Tissue Engineering and Regenerative Medicine
- Genomics, phytochemicals, and oxidative stress
- Energy and Environment Impacts
- Stress Responses and Cortisol
- Electron Spin Resonance Studies
- Plant tissue culture and regeneration
- Hormonal Regulation and Hypertension
- Climate Change and Health Impacts
- Energy, Environment, and Transportation Policies
Institut Supérieur des Biotechnologies de Paris
2021-2023
Université Paris Cité
2023
Institut Pasteur
2015-2023
Centre National de la Recherche Scientifique
2017-2023
Institut des Cellules Souches pour le Traitement et l'Étude des Maladies Monogéniques
2021
Université de Rouen Normandie
2015-2021
Université de Caen Normandie
2020
Normandie Université
2020
Biologie du Développement et Cellules Souches
2019
Aliments Bioprocédés Toxicologie Environnements
2012-2018
Abstract Sepsis, or systemic inflammatory response syndrome, is the major cause of critical illness resulting in admission to intensive care units. Sepsis caused by severe infection and associated with mortality 60% cases. Morbidity due sepsis complicated neuromyopathy, patients face long-term disability muscle weakness, energetic dysfunction, proteolysis wasting. These processes are triggered pro-inflammatory cytokines metabolic imbalances aggravated malnutrition drugs. Skeletal...
Abstract Cellular senescence has causative links with ageing and age-related diseases, however, it remains unclear if progeroid factors cause in normal cells. Here, we show that depletion of CSB, a protein mutated Cockayne syndrome (CS), is the earliest known trigger p21-dependent replicative senescence. CSB promotes overexpression HTRA3 protease resulting mitochondrial impairments, which are causally linked to CS pathological phenotypes. The promoter downregulated by histone H3...
In post-menopausal women, incidence of heart failure with preserved ejection fraction is higher than in men. Hormonal replacement therapies did not demonstrate benefits. We tested whether the non-steroidal mineralocorticoid receptor antagonist finerenone limits progression ovariectomized (OVX) mice metabolic disorders.
Cardiac subsarcolemmal mitochondria (SSM) and interfibrillar (IFM) subpopulations display distinct biochemical, morphological, functional characteristics. Moreover, they appear to be differently influenced during cardiac pathologies or toxic injuries. Although mitochondrial reactive oxygen species seem play a critical role in function diseases, limited information exists about the superoxide production characteristics of these subpopulations. In this work, using direct measurement by...
Traffic air pollution is a major health problem and recognized as an important risk factor for cardiovascular (CV) diseases. In previous experimental study, we showed that diesel exhaust (DE) exposures induced cardiac mitochondrial CV dysfunctions associated with the gaseous phase. Here, hypothesized NO2 to levels close those found in DE induce reactive oxygen species (ROS) production, which contribute endothelial dysfunction, early indicator numerous For this, studied effects of on ROS...
Cockayne syndrome (CS) and UV-sensitive (UVSS) are rare genetic disorders caused by mutation of the DNA repair multifunctional CSA or CSB protein, but only CS patients display a progeroid neurodegenerative phenotype, providing unique conceptual experimental paradigm. As methylation (DNAm) remodelling is major ageing marker, we performed genome-wide analysis DNAm fibroblasts from healthy, UVSS individuals. Differential highlighted CS-specific epigenomic signature (progeroid-related; not...
Cockayne syndrome (CS) is a rare disease caused by mutations in ERCC6/CSB or ERCC8/CSA. We report here the clinical, genetic, and functional analyses of three unrelated patients mutated with severe phenotype. After clinical examination, two were investigated via next generation sequencing, targeting seventeen Nucleotide Excision Repair (NER) genes. All harbored novel, c.3156dup, homozygous mutation located exon 18 that affects C-terminal region protein. Sanger sequencing confirmed parental...
Abstract Cockayne syndrome (CS) and UV-sensitivity (UVSS) are rare genetic disorders caused by mutation of the DNA repair chromatin remodelling proteins CSA or CSB, but only CS patients display a progeroid neurodegenerative phenotype. As epigenetic modifications constitute well-established hallmark ageing, we characterized genome-wide methylation (DNAm) fibroblasts from versus UVSS healthy donors. The analysis differentially methylated positions regions revealed CS-specific signature,...