Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Mar 28;12(4):509. doi: 10.3390/biom12040509

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 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/).

PMC Copyright notice

Diagram depicting mechanisms by which endothelial dysfunction contributes to AAA growth, including eNOS uncoupling, a phenotypic switch to a pro-thrombotic, pro-adhesive, permeable state in the setting of altered biomechanical stress, and EC stress generated by intraluminal thrombus accumulation. EC populations 1 and 2 as determined by single-cell RNA sequencing are shown in distinct colors (pink, purple) in low (light) and high (dark) stress states. Potential biomarkers (circulating TM, CCL2, EPCs, and FMD analysis) are depicted. Tobacco use is highlighted as a clinical risk factor for endothelial dysfunction and AAA progression. Abbreviations: AAA (abdominal aortic aneurysm); ARG (arginine); CCL20 (C-C Motif Chemokine Ligand 20); CIT (citrulline); EC (endothelial cell); eNOS (endothelial nitric oxide synthase); EPC (endothelial progenitor cell); FMD (flow mediated dilation); MMP (matrix metalloproteinase); NO (nitric oxide); TM (thrombomodulin).