Identifying novel mechanisms of abdominal aortic aneurysm
angiotensin II
elastase
inflammation
mouse model
network analysis
thrombosis
Journal
Frontiers in cardiovascular medicine
ISSN: 2297-055X
Titre abrégé: Front Cardiovasc Med
Pays: Switzerland
ID NLM: 101653388
Informations de publication
Date de publication:
2022
2022
Historique:
received:
04
03
2022
accepted:
28
06
2022
entrez:
22
8
2022
pubmed:
23
8
2022
medline:
23
8
2022
Statut:
epublish
Résumé
Abdominal aortic aneurysm (AAA), characterized by a continued expansion of the aorta, leads to rupture if not surgically repaired. Mice aid the study of disease progression and its underlying mechanisms since sequential studies of aneurysm development are not feasible in humans. The present study used unbiased proteomics and systems biology to understand the molecular relationship between the mouse models of AAA and the human disease. Aortic tissues of developing and established aneurysms produced by either angiotensin II (AngII) infusion in Identifying changes unique to each mouse model will help to contextualize model-specific findings. Focusing on shared proteins between mouse experimental models or between mouse and human tissues may help to better understand the mechanisms for AAA and establish molecular bases for novel therapies.
Sections du résumé
Background
UNASSIGNED
Abdominal aortic aneurysm (AAA), characterized by a continued expansion of the aorta, leads to rupture if not surgically repaired. Mice aid the study of disease progression and its underlying mechanisms since sequential studies of aneurysm development are not feasible in humans. The present study used unbiased proteomics and systems biology to understand the molecular relationship between the mouse models of AAA and the human disease.
Methods and results
UNASSIGNED
Aortic tissues of developing and established aneurysms produced by either angiotensin II (AngII) infusion in
Conclusions
UNASSIGNED
Identifying changes unique to each mouse model will help to contextualize model-specific findings. Focusing on shared proteins between mouse experimental models or between mouse and human tissues may help to better understand the mechanisms for AAA and establish molecular bases for novel therapies.
Identifiants
pubmed: 35990960
doi: 10.3389/fcvm.2022.889994
pmc: PMC9382335
doi:
Types de publication
Journal Article
Langues
eng
Pagination
889994Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL134892
Pays : United States
Informations de copyright
Copyright © 2022 Morgan, Lee, Halu, Nicolau, Higashi, Ha, Wen, Daugherty, Libby, Cameron, Mix, Aikawa, Owens, Singh and Aikawa.
Déclaration de conflit d'intérêts
Author HH is an employee of Kowa and was visiting scientist at Brigham and Women's Hospital when the study was conducted. Author MA has received research grants from Pfizer and Sanofi. Author PL is an unpaid consultant to or involved in clinical trials for Amgen, AstraZeneca, Esperion Therapeutics, Ionis Pharmaceuticals, Kowa, Novartis, Pfizer, Sanofi-Regeneron, and XBiotech, is a member of scientific advisory board for Amgen, Corvidia Therapeutics, DalCor Pharmaceuticals, IFM Therapeutics, Kowa, Olatec Therapeutics, Medimmune, Novartis, and XBiotech, and serves on the Board of XBiotech. The laboratory of PL has received research funding in the last 2 years from Novartis. Author PL has a financial interest in Xbiotech. His interests were reviewed and are managed by Brigham and Women's Hospital and Partners HealthCare in accordance with their conflict of interest policies. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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