Conference item : Abstract
Wnt5a contributes to human atherosclerosis via novel USP17 redox signalling
- Abstract:
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Background
Wnt5a is a non-canonical Wnt ligand with potential vascular effects, but its mechanistic role in atherosclerosis progression and the underlying downstream mechanisms are poorly explored.
Purpose
To address the hypothesis that Wnt5a induces vascular NADPH-oxidases activity, endothelial dysfunction and detrimental downstream redox signalling which could propagate atherosclerosis in humans.
Methods
Expand abstract
- Publication status:
- Published
- Peer review status:
- Reviewed (other)
Actions
Access Document
- Files:
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(Preview, Accepted manuscript, pdf, 277.8KB, Terms of use)
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- Publisher copy:
- 10.1093/eurheartj/ehz748.1026
Authors
- Publisher:
- Oxford University Press
- Journal:
- European Heart Journal More from this journal
- Volume:
- 40
- Issue:
- S1
- Pages:
- 1660
- Publication date:
- 2019-10-21
- Event title:
- ESC Congress 2019 together with World Congress of Cardiology
- Event location:
- Paris, France
- Event website:
- https://www.escardio.org/Congresses-&-Events/ESC-Congress
- Event start date:
- 2019-08-31
- Event end date:
- 2019-09-04
- DOI:
- EISSN:
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1522-9645
- ISSN:
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0195-668X
- Language:
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English
- Keywords:
- Subtype:
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Abstract
- Pubs id:
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1084314
- Local pid:
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pubs:1084314
- Deposit date:
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2020-02-10
- ARK identifier:
Terms of use
- Copyright holder:
- Akoumianakis et al.
- Copyright date:
- 2019
- Rights statement:
- Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2019. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model.
- Notes:
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This paper was presented at the ESC Congress 2019 together with World Congress of Cardiology, 31 August – 4 September 2019, Paris, France. This is the accepted manuscript version of the paper. The final version is available online from Oxford University Press at: https://doi.org/10.1093/eurheartj/ehz748.1026
- Licence:
- Other
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