Zobrazeno 1 - 10
of 59
pro vyhledávání: '"Philipp Skroblin"'
Autor:
Amy J. Osborne, Agnieszka Bierzynska, Elizabeth Colby, Uwe Andag, Philip A. Kalra, Olivier Radresa, Philipp Skroblin, Maarten W. Taal, Gavin I. Welsh, Moin A. Saleem, Colin Campbell
Publikováno v:
npj Systems Biology and Applications, Vol 10, Iss 1, Pp 1-15 (2024)
Abstract Chronic kidney diseases (CKD) have genetic associations with kidney function. Univariate genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with estimated glomerular filtration rate (eGFR
Externí odkaz:
https://doaj.org/article/720dcb90cc644525b4ddd6be5815d98b
Autor:
Victoria Ulrich, Noemi Rotllan, Elisa Araldi, Amelia Luciano, Philipp Skroblin, Mélanie Abonnenc, Paola Perrotta, Xiaoke Yin, Ashley Bauer, Kristen L Leslie, Pei Zhang, Binod Aryal, Rusty L Montgomery, Thomas Thum, Kathleen Martin, Yajaira Suarez, Manuel Mayr, Carlos Fernandez‐Hernando, William C Sessa
Publikováno v:
EMBO Molecular Medicine, Vol 8, Iss 6, Pp 643-653 (2016)
Abstract Abnormal remodeling of atherosclerotic plaques can lead to rupture, acute myocardial infarction, and death. Enhancement of plaque extracellular matrix (ECM) may improve plaque morphology and stabilize lesions. Here, we demonstrate that chron
Externí odkaz:
https://doaj.org/article/dfae49429d474f239ee09a30e0002d2d
Autor:
Tobias Bohnenpoll, Eric Olson, Mykola Dergai, Jennifer Cox, Simone Romoli, I-Ju Lo, Johannes Pospiech, Krishan Vishnolia, Mark Mcconnell, Marvin Gunawan, Michaela Bayerlová, Nicolette Honson, Niklas Michel, Nikolas Stroth, Olivier Radresa, Philipp Skroblin, Priyanka Kohli, Seamus Ragan, Shenshen Lai, Steven Bromidge, David Powell, Uwe Andag, Andrew King
Publikováno v:
Nephrology Dialysis Transplantation. 37
BACKGROUND Conventional stratification by clinical and histopathological phenotypes only approximates the heterogeneity of chronic kidney disease (CKD) and is insufficient to drive discovery of disease-modifying therapies or predict clinical outcomes
Autor:
Ruifang Lu, Sanjay Sinha, Dieter P. Reinhardt, Shaynah Wanga, Adam Lee Fellows, Marjan Jahangiri, Vivian de Waard, Maarten Groenink, Javier Barallobre-Barreiro, Carlie J.M. de Vries, Barbara J.M. Mulder, Romy Franken, David R. Koolbergen, Rosa Viner, Manuel Mayr, Xiaoke Yin, Qiuru Xing, Aeilko H. Zwinderman, Ron Balm, Ferheen Baig, Philipp Skroblin, Hongorzul Davaapil, Marika Fava
Publikováno v:
Yin, X, Wanga, S, Fellows, A L, Barallobre-Barreiro, J, Lu, R, Davaapil, H, Franken, R, Fava, M, Baig, F, Skroblin, P, Xing, Q, Koolbergen, D R, Groenink, M, Zwinderman, A H, Balm, R, de Vries, C J M, Mulder, B J M, Viner, R, Jahangiri, M, Reinhardt, D P, Sinha, S, de Waard, V & Mayr, M 2019, ' Glycoproteomic Analysis of the Aortic Extracellular Matrix in Marfan Patients. ', Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 39, no. 9, pp. 1859–1873 . https://doi.org/10.1161/ATVBAHA.118.312175
Arteriosclerosis, Thrombosis, and Vascular Biology
Arteriosclerosis, thrombosis, and vascular biology, 39(9), 1859-1873. Lippincott Williams and Wilkins
Arteriosclerosis, Thrombosis, and Vascular Biology
Arteriosclerosis, thrombosis, and vascular biology, 39(9), 1859-1873. Lippincott Williams and Wilkins
Supplemental Digital Content is available in the text.
Objective: Marfan syndrome (MFS) is caused by mutations in FBN1 (fibrillin-1), an extracellular matrix (ECM) component, which is modified post-translationally by glycosylation. This study ai
Objective: Marfan syndrome (MFS) is caused by mutations in FBN1 (fibrillin-1), an extracellular matrix (ECM) component, which is modified post-translationally by glycosylation. This study ai
Autor:
Ruifang Lu, Philipp Skroblin, Gerard Pasterkamp, Sarah R. Langley, Catherine M. Shanahan, Peter Willeit, Mariette Lengquist, Chris Molenaar, Joseph Shalhoub, Manuel Mayr, Alexander N. Kapustin, Ljubica Perisic Matic, Karin Willeit, Ulf Hedin, Claudia Monaco, Johann Willeit, Athanasios Didangelos, Bernhard Iglseder, Temo Barwari, Stefan Kiechl, Xiaoke Yin, Bernhard Paulweber, Javier Barallobre-Barreiro, Alun H. Davies, Ludmilla Kedenko, Gonca Suna, Gregor Rungger
Publikováno v:
The Journal of Clinical Investigation
Journal of Clinical Investigation, 127(4), 1546. The American Society for Clinical Investigation
Langley, S R, Willeit, K, Didangelos, A, Matic, L P, Skroblin, P, Barallobre-barreiro, J, Lengquist, M, Rungger, G, Kapustin, A, Kedenko, L, Molenaar, C, Lu, R, Barwari, T, Suna, G, Yin, X, Iglseder, B, Paulweber, B, Willeit, P, Shalhoub, J, Pasterkamp, G, Davies, A H, Monaco, C, Hedin, U, Shanahan, C M, Willeit, J, Kiechl, S & Mayr, M 2017, ' Extracellular matrix proteomics identifies molecular signature of symptomatic carotid plaques ', Journal of Clinical Investigation, vol. 127, no. 4, pp. 1546-1560 . https://doi.org/10.1172/JCI86924
Journal of Clinical Investigation, 127(4), 1546. The American Society for Clinical Investigation
Langley, S R, Willeit, K, Didangelos, A, Matic, L P, Skroblin, P, Barallobre-barreiro, J, Lengquist, M, Rungger, G, Kapustin, A, Kedenko, L, Molenaar, C, Lu, R, Barwari, T, Suna, G, Yin, X, Iglseder, B, Paulweber, B, Willeit, P, Shalhoub, J, Pasterkamp, G, Davies, A H, Monaco, C, Hedin, U, Shanahan, C M, Willeit, J, Kiechl, S & Mayr, M 2017, ' Extracellular matrix proteomics identifies molecular signature of symptomatic carotid plaques ', Journal of Clinical Investigation, vol. 127, no. 4, pp. 1546-1560 . https://doi.org/10.1172/JCI86924
Background The identification of patients with high-risk atherosclerotic plaques prior to the manifestation of clinical events remains challenging. Recent findings question histology- and imaging-based definitions of the "vulnerable plaque," necessit
Autor:
Mélanie Abonnenc, Pei Zhang, Victoria Ulrich, Yajaira Suárez, Kathleen A. Martin, Rusty L. Montgomery, Paola Perrotta, Thomas Thum, Kristen L. Leslie, Elisa Araldi, Philipp Skroblin, Amelia K. Luciano, Noemi Rotllan, Carlos Fernández-Hernando, William C. Sessa, Ashley J. Bauer, Manuel Mayr, Xiaoke Yin, Binod Aryal
Publikováno v:
EMBO Molecular Medicine
Abnormal remodeling of atherosclerotic plaques can lead to rupture, acute myocardial infarction, and death. Enhancement of plaque extracellular matrix (ECM) may improve plaque morphology and stabilize lesions. Here, we demonstrate that chronic admini
Publikováno v:
Journal of the American College of Cardiology. 67(7):813-816
One of the most challenging aspects of obesity is its link to “metabolic syndrome,” when abdominal obesity is accompanied by high fasting blood glucose, low levels of high-density lipoprotein cholesterol, high levels of triglycerides, and elevate
Autor:
Dorothee Kaudewitz, Herbert Tilg, Peter Santer, Alun D. Hughes, Carlos Fernández-Hernando, Philipp Skroblin, Manuel Mayr, Meredith Whitehead, Noemi Rotllan, Leigh Goedeke, Johann Willeit, Alexander R. Moschen, Temo Barwari, Stefan Kiechl, Peter Willeit, Xiaoke Yin, Cristina M. Ramírez, Enzo Bonora, Anna Zampetaki
Publikováno v:
Willeit, P, Skroblin, P, Moschen, A R, Yin, X, Kaudewitz, D, Zampetaki, A, Barwari, T, Whitehead, M, Ramírez, C M, Goedeke, L, Rotllan, N, Bonora, E, Hughes, A D, Santer, P, Fernández-Hernando, C, Tilg, H, Willeit, J, Kiechl, S & Mayr, M 2017, ' Circulating MicroRNA-122 is associated with the risk of new-onset metabolic syndrome and type 2 diabetes ', Diabetes, vol. 66, no. 2, pp. 347-357 . https://doi.org/10.2337/db16-0731
MicroRNA-122 (miR-122) is abundant in the liver and involved in lipid homeostasis, but its relevance to the long-term risk of developing metabolic disorders is unknown. We therefore measured circulating miR-122 in the prospective population-based Bru
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2bef097d853e66f2113e9e86c888d643
https://kclpure.kcl.ac.uk/ws/files/147329856/Circulating_MicroRNA_122_ZAMPETAKI_Publishedonline29November2016_GREEN_AAM.pdf
https://kclpure.kcl.ac.uk/ws/files/147329856/Circulating_MicroRNA_122_ZAMPETAKI_Publishedonline29November2016_GREEN_AAM.pdf
Publikováno v:
PROTEOMICS - Clinical Applications. 7:504-515
Aortic aneurysm is a deceptively indolent disease that can cause severe complications such as aortic rupture and dissection. In the normal aorta, vascular smooth muscle cells within the medial layer produce and sustain the extracellular matrix (ECM)
Autor:
Philipp Skroblin, Enno Klussmann, Michelle L. Halls, Antonio Ciruela, Katy L. Everett, Debbie Willoughby, Dermot M.F. Cooper
Publikováno v:
Journal of cell science, 125: 5850-5859
Summary Adenylyl cyclase (AC) isoforms can participate in multimolecular signalling complexes incorporating A-kinase anchoring proteins (AKAPs). We recently identified a direct interaction between Ca2+-sensitive AC8 and plasma membrane-targeted AKAP7