A5078122219- Muscle Physiology and Disorders
- Adipose Tissue and Metabolism
- Atherosclerosis and Cardiovascular Diseases
- Signaling Pathways in Disease
- Immune cells in cancer
- Metabolism, Diabetes, and Cancer
- Cardiac Fibrosis and Remodeling
- Receptor Mechanisms and Signaling
- Autophagy in Disease and Therapy
- Nutrition and Health in Aging
- Inflammation biomarkers and pathways
- Muscle metabolism and nutrition
- Dietary Effects on Health
- Caveolin-1 and cellular processes
- Sports and Physical Education Research
- Diabetes Treatment and Management
- Pancreatic and Hepatic Oncology Research
- Chemokine receptors and signaling
- Diet, Metabolism, and Disease
- Kawasaki Disease and Coronary Complications
- Genetic Neurodegenerative Diseases
- Histone Deacetylase Inhibitors Research
- Apelin-related biomedical research
- Phagocytosis and Immune Regulation
- Genetics and Physical Performance
Paris Cardiovascular Research Center
2019-2024
Université Paris Cité
2019-2024
Instituto de Investigación Sanitaria de Santiago
2012-2024
Complejo Hospitalario Universitario de Santiago
2013-2024
Inserm
2019-2024
Sorbonne Paris Cité
2019-2021
Servicio Gallego de Salud
2013-2018
Centro de Investigación Biomédica en Red
2012-2015
Abstract Acute myocardial infarction is a common condition responsible for heart failure and sudden death. Here, we show that following acute in mice, CD8 + T lymphocytes are recruited activated the ischemic tissue release Granzyme B, leading to cardiomyocyte apoptosis, adverse ventricular remodeling deterioration of function. Depletion decreases apoptosis within myocardium, hampers inflammatory response, limits injury improves These effects recapitulated mice with B -deficient cells. The...
The triggering receptor expressed on myeloid cells 1 (TREM-1) drives inflammatory responses in several cardiovascular diseases but its role abdominal aortic aneurysm (AAA) remains unknown. Our objective was to explore the of TREM-1 a mouse model angiotensin II-induced (AngII-induced) AAA. expression detected and colocalized with macrophages. Trem1 gene deletion (Apoe-/-Trem1-/-), as well pharmacological blockade LR-12 peptide, limited both AAA development severity. attenuated response aorta,...
Abstract Caspase recruitment-domain containing protein 9 (CARD9) is a key signaling pathway in macrophages but its role atherosclerosis still poorly understood. Global deletion of Card9 Apoe -/- mice as well hematopoietic Ldlr increases atherosclerosis. The acceleration also observed Rag2 mice, ruling out for the adaptive immune system vascular phenotype deficient mice. deficiency alters macrophage through CD36 overexpression with increased IL-1β production, lipid uptake, higher cell death...
The development of therapeutic strategies for skeletal muscle diseases, such as physical injuries and myopathies, depends on the knowledge regulatory signals that control myogenic process. obestatin/GPR39 system operates an autocrine signal in regulation myogenesis. Using a mouse model regeneration after injury several cellular strategies, we explored potential use obestatin agent treatment trauma-induced injuries. Our results evidenced overexpression preproghrelin, thus obestatin, GPR39...
The growth hormone secretagogue receptor, GHSR1a, mediates the biological activities of ghrelin, which includes secretion hormone, as well stimulation appetite, food intake and maintenance energy homeostasis. Mapping phosphorylation sites on GHSR1a knowledge how these control specific functional consequences unlocks new strategies for development therapeutic agents targeting individual functions. Herein, we have identified different sets within engender distinct functionality ß-arrestins....
Defects in efficient endothelial healing have been associated with complication of atherosclerosis such as post-angioplasty neoatherosclerosis and plaque erosion leading to thrombus formation. However, current preventive strategies do not consider re-endothelialization their design. Here, we investigate mechanisms linking immune processes defect re-endothelialization. We especially evaluate if targeting phosphoinositide 3-kinase γ could restore identify mediators responsible for these...
Abstract Background Many pathological states characterized by muscle atrophy are associated with an increase in circulating glucocorticoids and poor patient prognosis, making it important target for treatment. The development of treatments glucocorticoid‐induced wasting disorder‐related skeletal should be designed based on how the particular transcriptional program is orchestrated balance protein synthesis degradation deregulated. Here, we investigated whether obestatin/GPR39 system,...
Abstract Background A therapeutic approach for the treatment of glucocorticoid‐induced skeletal muscle atrophy should be based on knowledge molecular mechanisms determining unbalance between anabolic and catabolic processes how to re‐establish this balance. Here, we investigated whether obestatin/GPR39 system, an autocrine signalling system acting myogenesis with effects muscle, could protect against chronic atrophy. Methods In study, used in vivo model induced by synthetic glucocorticoid...
BACKGROUND: The long isoform of the Wnk1 (with-no-lysine [K] kinase 1) is a ubiquitous serine/threonine kinase, but its role in vascular smooth muscle cells (VSMCs) pathophysiology remains unknown. METHODS: AngII (angiotensin II) was infused Apoe −/− to induce experimental aortic aneurysm. Mice carrying an Sm22-Cre allele were cross-bred with mice floxed specifically investigate functional VSMCs. RESULTS: Single-cell RNA-sequencing aneurysmal abdominal aorta from AngII-infused revealed that...
Obestatin/GPR39 signaling stimulates skeletal muscle growth and repair by inducing both G-protein-dependent -independent mechanisms linking the activated GPR39 receptor with distinct sets of accessory effector proteins. In this work, we describe a new level activity where obestatin plays role in formation, contractile properties metabolic profile through determination oxidative fiber type. Our data indicate that regulates Mef2 PGC-1α expression. Both result shift metabolism function. The...
Abstract Macrophage-mediated innate immune responses contribute to the initiation, progression and complications of atherosclerosis. However, underlying pathways linking activation macrophages atherosclerotic plaque develoment are still poorly understood. We hypothesized that caspase recruitment-domain containing protein 9 (CARD9) plays a determinant role in pro-atherogenic macrophages. showed global deletion Card9 male Apoe −/− mice as well hematopoietic female Ldlr increased chimeric...
Abstract Macrophage-mediated innate immune responses contribute to the initiation, progression and complications of atherosclerosis. However, underlying pathways linking activation macrophages atherosclerotic plaque develoment are still poorly understood. We hypothesized that caspase recruitment-domain containing protein 9 (CARD9) plays a determinant role in pro-atherogenic macrophages. showed global deletion Card9 male Apoe −/− mice as well hematopoietic female Ldlr increased chimeric...