3 results match your criteria: "Ludwig-Maximilians-University Munich and DZHK (German Centre for Cardiovascular Research)[Affiliation]"
Mechanical Activation of Hypoxia-Inducible Factor 1α Drives Endothelial Dysfunction at Atheroprone Sites.
Arterioscler Thromb Vasc Biol
November 2017
From the Department of Infection, Immunity, and Cardiovascular Disease, INSIGNEO Institute for In Silico Medicine, and the Bateson Centre (S.F., N.B., M.F., C.S., H.S., M.M., D.P., B.T.A., A.A.R.T., V.R., P.C.E.) and Sheffield Institute for Translational Neuroscience (S.A.), University of Sheffield, United Kingdom; Institute for Cardiovascular Prevention, Ludwig-Maximilians University of Munich and DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Germany (S.A., C.W., A.S.); and Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta (H.J.).
Objective: Atherosclerosis develops near branches and bends of arteries that are exposed to low shear stress (mechanical drag). These sites are characterized by excessive endothelial cell (EC) proliferation and inflammation that promote lesion initiation. The transcription factor HIF1α (hypoxia-inducible factor 1α) is canonically activated by hypoxia and has a role in plaque neovascularization.
View Article and Find Full Text PDFMicroRNA-mediated mechanisms of the cellular stress response in atherosclerosis.
Nat Rev Cardiol
June 2015
Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich and DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Pettenkoferstrasse 9, 80336 Munich, Germany.
Atherosclerosis is characterised by the accumulation of lipid-laden macrophages in atherosclerotic lesions and occurs preferentially at arterial branching points, which are prone to inflammation during hyperlipidaemic stress. The increased susceptibility at branching sites of arteries is attributable to poor adaptation of arterial endothelial cells to disturbed blood flow. In the past 5 years, several studies have provided mechanistic insights into the regulatory roles of microRNAs (miRNAs) in inflammatory activation, proliferation, and regeneration of endothelial cells during this maladaptive process.
View Article and Find Full Text PDFHigh-resolution imaging of intravascular atherogenic inflammation in live mice.
Circ Res
February 2014
From the Department of Epidemiology, Atherothrombosis, and Imaging, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain (R.C., J.M.G.-G., V.S., C.S.-R., P.M.-S., A.H., V.A.); Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich and DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany (R.T.A.M., C.W., O.S.); Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands (R.T.A.M., C.W.); and Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands (O.S.).
Rationale: The inflammatory processes that initiate and propagate atherosclerosis remain poorly understood, largely because defining the intravascular behavior of immune cells has been technically challenging. Respiratory and pulsatile movements have hampered in vivo visualization of leukocyte accumulation in athero-prone arteries at resolutions achieved in other tissues.
Objective: To establish and to validate a method that allows high-resolution imaging of inflammatory leukocytes and platelets within the carotid artery of atherosusceptible mice in vivo.