Dysregulations of Key Regulators of Angiogenesis and Inflammation in Abdominal Aortic Aneurysm

Abdominal aortic aneurysm (AAA) is a chronic vascular disease caused by localized weakening and broadening of the abdominal aorta. AAA is a clearly underdiagnosed disease and is burdened with a high mortality rate (65–85%) from AAA rupture. Studies indicate that abnormal regulation of angiogenesis a...

Full description

Saved in:
Bibliographic Details
Published inInternational journal of molecular sciences Vol. 24; no. 15; p. 12087
Main Authors Zalewski, Daniel, Chmiel, Paulina, Kołodziej, Przemysław, Borowski, Grzegorz, Feldo, Marcin, Kocki, Janusz, Bogucka-Kocka, Anna
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 28.07.2023
MDPI
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Abdominal aortic aneurysm (AAA) is a chronic vascular disease caused by localized weakening and broadening of the abdominal aorta. AAA is a clearly underdiagnosed disease and is burdened with a high mortality rate (65–85%) from AAA rupture. Studies indicate that abnormal regulation of angiogenesis and inflammation contributes to progression and onset of this disease; however, dysregulations in the molecular pathways associated with this disease are not yet fully explained. Therefore, in our study, we aimed to identify dysregulations in the key regulators of angiogenesis and inflammation in patients with AAA in peripheral blood mononuclear cells (using qPCR) and plasma samples (using ELISA). Expression levels of ANGPT1, CXCL8, PDGFA, TGFB1, VEGFB, and VEGFC and plasma levels of TGF-alpha, TGF-beta 1, VEGF-A, and VEGF-C were found to be significantly altered in the AAA group compared to the control subjects without AAA. Associations between analyzed factors and risk factors or biochemical parameters were also explored. Any of the analyzed factors was associated with the size of the aneurysm. The presented study identified dysregulations in key angiogenesis- and inflammation-related factors potentially involved in AAA formation, giving new insight into the molecular pathways involved in the development of this disease and providing candidates for biomarkers that could serve as diagnostic or therapeutic targets.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
M.F., J.K. and A.B.-K. shared senior authorship.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms241512087