Publications by authors named "S Renet"
Article Synopsis
- The study explores how altered endothelial flow sensitivity related to polycystin deficiency contributes to hypertension in autosomal dominant polycystic kidney disease (ADPKD) patients.
- Nineteen ADPKD patients were treated with the dopamine receptor agonist rotigotine, showing that a higher dose significantly improved nitric oxide release and endothelial function without major changes in overall blood pressure.
- The findings suggest that targeting endothelial dopamine receptors could be a promising new treatment strategy to mitigate cardiovascular issues linked with ADPKD.
Introduction: Links have been established between SARS-CoV-2 and endoplasmic reticulum stress (ERS). However, the relationships between inflammation, ERS, and the volume of organ damage are not well known in humans. The aim of this study was to explore whether ERS explains lung damage volume (LDV) among COVID-19 patients admitted to the intensive care unit (ICU).
View Article and Find Full Text PDFEpigenetic regulation of histone H3K27 methylation has recently emerged as a key step during alternative immunoregulatory M2-like macrophage polarization; known to impact cardiac repair after Myocardial Infarction (MI). We hypothesized that EZH2, responsible for H3K27 methylation, could act as an epigenetic checkpoint regulator during this process. We demonstrate for the first time an ectopic EZH2, and putative, cytoplasmic inactive localization of the epigenetic enzyme, during monocyte differentiation into M2 macrophages in vitro as well as in immunomodulatory cardiac macrophages in vivo in the post-MI acute inflammatory phase.
View Article and Find Full Text PDFIntroduction: Although the physiological role of the C-terminal hydrolase domain of the soluble epoxide hydrolase (sEH-H) is well investigated, the function of its N-terminal phosphatase activity (sEH-P) remains unknown.
Objectives: This study aimed to assess in vivo the physiological role of sEH-P.
Methods: CRISPR/Cas9 was used to generate a novel knock-in (KI) rat line lacking the sEH-P activity.
Background: We hypothesized that supraceliac aortic cross clamping could induce lung injury mediated by an inflammatory ischemia-reperfusion (IR) trigger. We aimed to characterize glycocalyx (GCX), a component of endothelial membrane, participating to remote lung injury.
Methods: Rats underwent supraceliac aortic cross clamping for 40 min and were sacrificed at 0, 3, 6, and 24 hr of reperfusion (n = 10/group).