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© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.

Abstract

Peripheral artery disease (PAD) is prevalent among individuals with a history of tobacco smoking. Although oxidation of lipids may contribute to atherogenesis in vascular disease, enzymatically and nonenzymatically produced oxidized lipids can have varying and contrasting physiological effects. The underlying mechanisms of atherogenic vulnerability can be better elucidated with the recent advances in oxylipidome quantification using HPLC-MS/MS technology. In a randomized, controlled clinical trial, the plasma oxylipidome was analyzed in participants living with PAD by smoking status (n = 98) and in nonsmoking comparators without chronic disease (n = 20). Individuals with PAD had approximately a four-fold higher level of total plasma oxylipins versus the comparator. Cessation of smoking in individuals with PAD was associated with significantly lower levels of linoleic acid-derived TriHOMEs, greater levels of omega-3 fatty acid-derived oxylipins, and greater levels of nonfragmented oxidized phosphatidylcholines (OxPCs). Individuals living with PAD but without a history of smoking, exhibited higher levels of the putative atherogenic fragmented OxPCs versus individuals who currently or previously smoked. These data implicate the plasma oxylipidome in PAD and that smoking cessation is associated with a less inflammatory profile. Furthermore, fragmented OxPCs may play a more significant role in the pathophysiology of PAD in individuals without a history of smoking.

Details

Title
The Plasma Oxylipidome Links Smoking Status to Peripheral Artery Disease
Author
Caligiuri, Stephanie P B 1   VIAFID ORCID Logo  ; Pierce, Grant N 2   VIAFID ORCID Logo  ; Ravandi, Amir 3 ; Aukema, Harold M 4   VIAFID ORCID Logo 

 Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA 
 Canadian Centre for Agri-Food Research in Health and Medicine, Albrechtsen Research Centre, St. Boniface Hospital, Winnipeg, MB R2H 2A6, Canada; [email protected] (G.N.P.); [email protected] (H.M.A.); Institute of Cardiovascular Sciences, Albrechtsen Research Centre, St. Boniface Hospital, Winnipeg, MB R2H 2A6, Canada; [email protected]; Department of Physiology and Pathophysiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada 
 Institute of Cardiovascular Sciences, Albrechtsen Research Centre, St. Boniface Hospital, Winnipeg, MB R2H 2A6, Canada; [email protected]; Department of Physiology and Pathophysiology, University of Manitoba, Winnipeg, MB R3E 0J9, Canada; Department of Internal Medicine, University of Manitoba, Winnipeg, MB R3E 0Z2, Canada 
 Canadian Centre for Agri-Food Research in Health and Medicine, Albrechtsen Research Centre, St. Boniface Hospital, Winnipeg, MB R2H 2A6, Canada; [email protected] (G.N.P.); [email protected] (H.M.A.); Department of Food and Human Nutritional Sciences, University of Manitoba, Winnipeg, MB R3T 6C5, Canada 
First page
627
Publication year
2022
Publication date
2022
Publisher
MDPI AG
e-ISSN
22181989
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2694020237
Copyright
© 2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.