A5077221124- Hormonal Regulation and Hypertension
- Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Ion Transport and Channel Regulation
- Cardiovascular Function and Risk Factors
- Electrolyte and hormonal disorders
- Protein Tyrosine Phosphatases
- ATP Synthase and ATPases Research
- Stress Responses and Cortisol
- Selenium in Biological Systems
- Lymphatic System and Diseases
- Cardiovascular Health and Disease Prevention
- Galectins and Cancer Biology
- Apelin-related biomedical research
- Estrogen and related hormone effects
- Pancreatic function and diabetes
- Coenzyme Q10 studies and effects
- Heart Failure Treatment and Management
- Nitric Oxide and Endothelin Effects
- Eicosanoids and Hypertension Pharmacology
- Menopause: Health Impacts and Treatments
- Muscle metabolism and nutrition
- Chronic Kidney Disease and Diabetes
- Macrophage Migration Inhibitory Factor
- Sodium Intake and Health
- Acute Kidney Injury Research
Inserm
2013-2024
Université de Rouen Normandie
2012-2023
Normandie Université
2018-2021
Endothélium, valvulopathies et insuffisance cardiaque
2021
Université Paris Cité
2005-2017
Sorbonne Université
2013-2017
Centre de Recherche des Cordeliers
2013-2017
Bayer (Germany)
2016-2017
Navarrabiomed
2017
Navarre Institute of Health Research
2017
Background— Life-threatening cardiac arrhythmia is a major source of mortality worldwide. Besides rare inherited monogenic diseases such as long-QT or Brugada syndromes, which reflect abnormalities in ion fluxes across channels final common pathway, arrhythmias are most frequently acquired and associated with heart disease. The mineralocorticoid hormone aldosterone an important contributor to morbidity failure, but its mechanisms action incompletely understood. Methods Results— To...
Arterial stiffness is recognized as a risk factor for many cardiovascular diseases. Aldosterone via its binding to and activation of the mineralocorticoid receptors (MRs) main regulator blood pressure by controlling renal sodium reabsorption. Although both clinical experimental data indicate that MR aldosterone involved in arterial stiffening, molecular mechanism not known. In addition kidney, expressed endothelial vascular smooth muscle cells (VSMCs), but specific contribution VSMC...
Inappropriate mineralocorticoid receptor (MR) activation is involved in cardiac diseases. Whether and how aldosterone the deleterious effects of still unclear. Mice overexpressing MR cardiomyocytes their controls were treated for 7 days with aldosterone, transcriptome was analyzed. Aldosterone regulated 265 genes cardiomyocyte-targeted overexpression mice. Forty three these also differentially expressed between untreated mice, thus representing putative aldosterone-regulated cardiomyocytes....
Mineralocorticoid receptor (MR) antagonists slow down the progression of heart failure after myocardial infarction (MI), but cell-specific role MR in these benefits is unclear. In this study, expressed vascular smooth muscle cells (VSMCs) was investigated. Two months coronary artery ligation causing MI, mice with VSMC-specific deletion (MI-MR(SMKO)) and treated antagonist finerenone (MI-fine) had improved left ventricular compliance elastance when compared infarcted control (MI-CTL), as well...
Myocardial infarction (MI) is accompanied by cardiac fibrosis, which contributes to dysfunction. Mineralocorticoid receptor (MR) antagonists have beneficial effects in patients with left ventricular (LV) dysfunction after MI. We herein investigated the role of MR target NGAL (neutrophil gelatinase–associated lipocalin) post-MI damages. Both higher baseline and a greater increase serum levels during follow-up were significantly associated lower 6-month LV ejection fraction recovery cohort 119...
Lymphatics are essential for cardiac health, and insufficient lymphatic expansion (lymphangiogenesis) contributes to development of heart failure (HF) after myocardial infarction. However, the regulation impact lymphangiogenesis in non-ischaemic cardiomyopathy following pressure-overload remains be determined. Here, we investigated transversal aortic constriction (TAC) C57Bl/6 Balb/c mice, end-stage HF patients.Cardiac function was evaluated by echocardiography, hypertrophy, lymphatics,...
The protein tyrosine phosphatase 1B (PTP1B) modulates kinase receptors, among which is the vascular endothelial growth factor receptor type 2 (VEGFR2), a key component of angiogenesis. Because PTP1B deficiency in mice improves left ventricular (LV) function mo after myocardial infarction (MI), we hypothesized that enhanced angiogenesis early MI via activated VEGFR2 contributes to this improvement. At 3 d MI, capillary density was increased at infarct border PTP1B–/– [+ 7±2% vs. wild-type...
Abstract Although optimal therapy for myocardial infarction includes reperfusion to restore blood flow the ischemic region, ischemia/reperfusion (IR) also initiates an inflammatory response likely contributing adverse left ventricular (LV) extracellular matrix (ECM) remodeling. Galectin-3 (Gal-3), a β-galactoside-binding-lectin, promotes cardiac remodeling and dysfunction. Our aim is investigate whether Gal-3 pharmacological inhibition using modified citrus pectin (MCP) improves functional...
Cardiac failure is a common feature in the evolution of cardiac disease. Among determinants failure, renin-angiotensin-aldosterone system has central role, and antagonism mineralocorticoid receptor (MR) been proposed as therapeutic strategy. In this study, we questioned role MR, not aldosterone, on heart function, using an inducible cardiac-specific transgenic mouse model. We have generated conditional knock-down model by expressing solely antisense mRNA directed against murine transcription...
The deleterious effects of aldosterone excess demonstrated in cardiovascular diseases might be linked part to coronary vascular dysfunction. However, whether such dysfunction is a cause or consequence the changes occurring cardiomyocytes unclear. Moreover, possible link between mineralocorticoid receptor (MR)-mediated on cardiomyocyte and arteries unknown. Thus we used mouse model with conditional, cardiomyocyte-specific overexpression human MR (hMR) observed endothelial function isolated...
This study addressed the hypothesis that inhibiting soluble epoxide hydrolase (sEH)-mediated degradation of epoxy-fatty acids, notably epoxyeicosatrienoic has an additional impact against cardiovascular damage in insulin resistance, beyond its previously demonstrated beneficial effect on glucose homeostasis. The and metabolic effects sEH inhibitor trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB; 10 mg/l drinking water) were compared with those sulfonylurea...
Aim To determine whether non‐steroidal mineralocorticoid receptor (MR) antagonists oppose metabolic syndrome‐related end‐organ, i.e. cardiac, damage. Materials and methods In Zucker fa/fa rats, a rat model of syndrome, we assessed the effects MR antagonist finerenone (oral 2 mg/kg/day) on left ventricular (LV) function, haemodynamics remodelling (using echocardiography, magnetic resonance imaging biochemical methods). Results Long‐term (90 days) modified neither systolic blood pressure nor...
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.
The mineralocorticoid receptor (MR) is a major regulator of renal sodium reabsorption and body fluid homeostasis. However, little known about glucocorticoid (GR)-dependent effects. Glucocorticoids may activate both receptors, so it difficult to distinguish between MR- GR-mediated effects in vivo. To overcome this complexity, we used transgenic mouse model allowing conditional GR overexpression (doxycycline inducible TetON system, Hoxb7 promoter) the collecting duct (CD) identify GR-regulated...
Abstract Neutrophil gelatinase-associated lipocalin (NGAL) is involved in cardiovascular and renal diseases. Gene inactivation of NGAL blunts the pathophysiological consequences damage. We aimed to design chemical inhibitors investigate its effects experimental models myocardial infarction (MI) chronic kidney disease induced by 5/6 nephrectomy (CKD) on respectively 8–12 weeks old C57Bl6/j FVB/N male mice. Among 32 tested, GPZ614741 GPZ058225 fully blocked NGAL-induced inflammatory...
Experimentally, aldosterone in association with NaCl induces cardiac fibrosis, oxidative stress, and inflammation through mineralocorticoid receptor activation; however, the biological processes regulated by alone heart remain to be identified.
Abstract Long-living individuals (LLIs) escape age-related cardiovascular complications until the very last stage of life. Previous studies have shown that a Longevity-Associated Variant (LAV) BPI Fold Containing Family B Member 4 ( BPIFB4 ) gene correlates with an extraordinarily prolonged life span. Moreover, delivery LAV-BPIFB4 exerted therapeutic action in murine models atherosclerosis, limb ischemia, diabetic cardiomyopathy, and aging. We hypothesize downregulation expression marks...
The renal collecting duct plays a key role in control of ion and fluid homeostasis. Genes encoding for transporters, hormone receptors, or regulatory proteins specifically expressed the are mutated several genetic diseases with altered blood pressure. Suitable cellular models expressing genes conditional way should represent attractive systems structure-function analyses generation appropriate physiopathological related diseases. However, such remains laborious quite inefficient. We adapted...
We have previously shown that protein tyrosine phosphatase 1B (PTP1B) inactivation in mice [PTP1B-deficient (PTP1B-/-) mice] improves left ventricular (LV) angiogenesis, perfusion, remodeling, and function limits endothelial dysfunction after myocardial infarction. However, whether PTP1B slows aging-associated cardiovascular remains unknown. Wild-type (WT) PTP1B-/- were allowed to age until 18 mo. Compared with old WT mice, which aging increased the LV mRNA expression of PTP1B, had 1)...