E
Ewa M. Paleolog
Researcher at University of Oxford
Publications - 118
Citations - 7162
Ewa M. Paleolog is an academic researcher from University of Oxford. The author has contributed to research in topics: Angiogenesis & Arthritis. The author has an hindex of 46, co-authored 118 publications receiving 6760 citations. Previous affiliations of Ewa M. Paleolog include Imperial College London & Arthritis Research UK.
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Journal ArticleDOI
Angiogenesis in rheumatoid arthritis
TL;DR: Although no clinical trials of anti-angiogenic therapy in RA have been reported to date, the blockade of angiogenesis – and especially of VEGF – appears to be a promising avenue for the future treatment of RA.
Journal ArticleDOI
Reduction of chemokine levels and leukocyte traffic to joints by tumor necrosis factor alpha blockade in patients with rheumatoid arthritis.
Peter C. Taylor,A. M. Peters,Ewa M. Paleolog,P T Chapman,M J Elliott,R V McCloskey,M Feldmann,Ravinder Nath Maini +7 more
TL;DR: TNFalpha blockade reduces synovial expression of the chemokines IL-8 and MCP-1 and diminishes inflammatory cell migration into RA joints and confirms the hypothesis that in rheumatoid arthritis, tumor necrosis factor alpha plays a critical role in regulating leukocyte trafficking and chemokine levels.
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Modulation of angiogenic vascular endothelial growth factor by tumor necrosis factor alpha and interleukin-1 in rheumatoid arthritis.
Ewa M. Paleolog,Sylvia Young,Alison C. Stark,Richard V. McCloskey,Marc Feldmann,Ravinder N. Maini +5 more
TL;DR: Inhibition of TNFalpha and IL-1 activity in vivo could reduce the drive to new blood vessel formation, and hence pannus mass, adding to other therapeutic effects of anti-TNFalpha therapy in RA.
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Canonical pathway of nuclear factor kappa B activation selectively regulates proinflammatory and prothrombotic responses in human atherosclerosis.
Claudia Monaco,Evangelos Andreakos,Serafim Kiriakidis,Claudia Mauri,Colin Bicknell,Brian M. J. Foxwell,Nicholas J.W. Cheshire,Ewa M. Paleolog,Marc Feldmann +8 more
TL;DR: The results demonstrate that the canonical pathway of NF-kappa B activation that involves p65, p50, c-Rel, and IKK-2 is activated in human atherosclerosis and results in selective up-regulation of major proinflammatory and prothrombotic mediators of the disease.
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Hypoxia--a key regulator of angiogenesis and inflammation in rheumatoid arthritis.
TL;DR: This Review highlights the molecular pathways activated by hypoxia, and how these pathways might interact with inflammatory signaling to promote and maintain synovitis in RA, with a particular focus on the response of macrophages to Hypoxia in the context of RA.