ArticlePloS one2011
Endothelial and macrophage-specific deficiency of P38α MAPK does not affect the pathogenesis of atherosclerosis in ApoE-/- mice.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Role of Mitogen-Activated Protein (MAP) Kinase Pathways in Metabolic Diseases.Genome integrity · 2024Review
- Smooth muscle cell specific NEMO deficiency inhibits atherosclerosis in ApoEScientific reports · 2022Article
- Urantide decreases hepatic steatosis in rats with experimental atherosclerosis via the MAPK/Erk/JNK pathway.Molecular medicine reports · 2021Article
- Update on Pharmacological Activities, Security, and Pharmacokinetics of Rhein.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- Sex as a Biological Variable in Atherosclerosis.Circulation research · 2020Review
- Role of p38 MAPK in Atherosclerosis and Aortic Valve Sclerosis.International journal of molecular sciences · 2018Review
- Flow signaling and atherosclerosis.Cellular and molecular life sciences : CMLS · 2017Review
- The role of mitogen-activated protein kinases and sterol receptor coactivator-1 in TGF-β-regulated expression of genes implicated in macrophage cholesterol uptake.Scientific reports · 2016Article
- Roles of p38α mitogen-activated protein kinase in mouse models of inflammatory diseases and cancer.The FEBS journal · 2015Review
- Myeloid-specific Krüppel-like factor 2 inactivation increases macrophage and neutrophil adhesion and promotes atherosclerosis.Circulation research · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe p38α Mitogen-Activated Protein Kinase (MAPK) regulates stress- and inflammation-induced cellular responses. Factors implicated in the development of atherosclerosis including modified low-density lipoprotein (LDL), cytokines and even shear stress induce p38 activation in endothelial cells and macrophages, which may be important for plaque formation. This study investigates the effects of endothelial- and macrophage-specific deficiency of p38α in atherosclerosis development, in Apolipoprotein E deficient (ApoE(-/-)) mice. METHODOLOGY/PRINCIPAL
findingsApoE(-/-) mice with macrophage or endothelial cell-specific p38α deficiency were fed a high cholesterol diet (HCD) for 10 weeks and atherosclerosis development was assessed by histological and molecular methods. Surprisingly, although p38α-deficiency strongly attenuated oxidized LDL-induced expression of molecules responsible for monocyte recruitment in endothelial cell cultures in vitro, endothelial-specific p38α ablation in vivo did not affect atherosclerosis development. Similarly, macrophage specific deletion of p38α did not affect atherosclerotic plaque development in ApoE(-/-) mice.
conclusionsAlthough previous studies implicated p38α signaling in atherosclerosis, our in vivo experiments suggest that p38α function in endothelial cells and macrophages does not play an important role in atherosclerotic plaque formation in ApoE deficient mice.
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