Publication
Mild endothelial dysfunction in Sirt3 knockout mice fed a high-cholesterol diet: protective role of a novel C/EBP-β-dependent feedback regulation of SOD2
Related publications (39)
Mitochondrial respiratory chain dysfunction disrupts intracellular cholesterol homeostasis
Mitochondrial diseases are rare and severe conditions with debilitating symptoms. Biochemical defects in mitochondria however are common. The difference between these two frequencies is suspected to lie in the capability of the cells to adapt to the homeos ...
EPFL2022Follicular regulatory helper T cells control the response of regulatory B cells to a high-cholesterol diet
Aims B cell functions in the process of atherogenesis have been investigated but several aspects remain to be clarified. Methods and results In this study, we show that follicular regulatory helper T cells (T-FR) control regulatory B cell (B-REG) populatio ...
OXFORD UNIV PRESS2021Mitochondrial Deacetylase Sirt3 Reduces Vascular Dysfunction and Hypertension While Sirt3 Depletion in Essential Hypertension Is Linked to Vascular Inflammation and Oxidative Stress
Rationale: Hypertension represents a major risk factor for stroke, myocardial infarction, and heart failure and affects 30% of the adult population. Mitochondrial dysfunction contributes to hypertension, but specific mechanisms are unclear. The mitochondri ...
2020Long noncoding RNA SNHG12 integrates a DNA-PK-mediated DNA damage response and vascular senescence
Johan Auwerx, Norman Lionel Moullan, Lei Chen
Long noncoding RNAs (lncRNAs) are emerging regulators of biological processes in the vessel wall; however, their role in atherosclerosis remains poorly defined. We used RNA sequencing to profile lncRNAs derived specifically from the aortic intima of Ldlr(- ...
AMER ASSOC ADVANCEMENT SCIENCE2020Cardiotrophin-1 Deficiency Abrogates Atherosclerosis Progression
Cardiotrophin-1 (CT-1) is associated with cardiovascular (CV) diseases. We investigated the effect of CT-1 deficiency in the development and progression of atherosclerosis in double knockout Apoe(-/-)ct-1(-/-) mice. Apoe(-/-) C57Bl/6 or Apoe(-/-)ct-1(-/-) ...
2020Role of ERK1/2 activation and nNOS uncoupling on endothelial dysfunction induced by lysophosphatidylcholine
Nikolaos Stergiopoulos, Luciano Dos Santos Aggum Capettini
Background and aims: Lysophosphatidylcholine (LPC) - a main component of oxidized LDL -is involved in endothelial dysfunction that precedes atherosclerosis, with an increased superoxide anions and a reduced NO production via endothelial NO synthase (eNOS) ...
Elsevier2017Treatment with the GPR55 antagonist CID16020046 increases neutrophil activation in mouse atherogenesis
Endocannabinoids modulate atherogenesis by triggering different receptors. Recently, orphan G protein-coupled receptors (GPRs) were suggested to be activated by endocannabinoids, possibly regulating vasorelaxation. Here, we investigated whether GPR55 antag ...
Schattauer Gmbh-Verlag Medizin Naturwissenschaften2016The Sirt1 activator SRT3025 provides atheroprotection in Apoe(-/-) mice by reducing hepatic Pcsk9 secretion and enhancing Ldlr expression
Johan Auwerx, Kristina Schoonjans, Matthias Alexander Sokrates Stein, Tasneem Arsiwala
The deacetylase sirtuin 1 (Sirt1) exerts beneficial effects on lipid metabolism, but its roles in plasma LDL-cholesterol regulation and atherosclerosis are controversial. Thus, we applied the pharmacological Sirt1 activator SRT3025 in a mouse model of athe ...
Oxford University Press2015Treatment with KLEPTOSE (R) CRYSMEB reduces mouse atherogenesis by impacting on lipid profile and Th1 lymphocyte response
The ability of pharmacological agents to target both "classical" risk factors and inflammation may be key for successful outcomes in the prevention and treatment of atherogenesis. Among the promising drugs interfering with cholesterol metabolism, we invest ...
Elsevier Science Inc2015Treatment with sulphated galactan inhibits macrophage chemotaxis and reduces intraplaque macrophage content in atherosclerotic mice
Experimental data from animal models and clinical studies support connections between the haemostasis and inflammation in atherogenesis. These interfaces among inflammation and thrombogenesis have been suggested as targets for pharmacological intervention ...
Elsevier Science Inc2015