Caitlyn Se
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Caitlyn Se has a total of 5 co-authors. Here are the top co-authors by number of shared publications:
- Amelia Stranz
Department of Surgery, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI 53726, USA
1 shared publication - Elise DeRoo
University of Wisconsin School of Medicine and Public Health, Madison, WI
1 shared publication - Huan Yang
Department of Surgery, University of Wisconsin, Madison, WI 53705, USA
1 shared publication - Marvin L. Hsieh
Institute of Biomedical Sciences, Academia Sinica, Taipei 115, Taiwan
1 shared publication - Ting Zhou
Department of Surgery, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, United States
1 shared publication
Latest Publications
- Open Access
- 28 March 2022
- Published by MDPI AG in Biomolecules
- Vol. 12 (4) , 509
Endothelial Dysfunction in the Pathogenesis of Abdominal Aortic Aneurysm
Abdominal aortic aneurysm (AAA), defined as a focal dilation of the abdominal aorta beyond 50% of its normal diameter, is a common and potentially life-threatening vascular disease. The molecular and cellular mechanisms underlying AAA pathogenesis remain unclear. Healthy endothelial cells (ECs) play a critical role in maintaining vascular homeostasis by regulating vascular tone and maintaining an anti-inflammatory, anti-thrombotic local environment. Increasing evidence indicates that endothelial dysfunction is an early pathologic event in AAA formation, contributing to both oxidative stress and inflammation in the degenerating arterial wall. Recent studies utilizing single-cell RNA sequencing revealed heterogeneous EC sub-populations, as determined by their transcriptional profiles, in aortic aneurysm tissue. This review summarizes recent findings, including clinical evidence of endothelial dysfunction in AAA, the impact of biomechanical stress on EC in AAA, the role of endothelial nitric oxide synthase (eNOS) uncoupling in AAA, and EC heterogeneity in AAA. These studies help to improve our understanding of AAA pathogenesis and ultimately may lead to the generation of EC-targeted therapeutics to treat or prevent this deadly disease.
- 28 March 2022
- Published by MDPI AG in Biomolecules
- Vol. 12 (4) , 509
Open AccessEndothelial Dysfunction in the Pathogenesis of Abdominal Aortic Aneurysm
Abdominal aortic aneurysm (AAA), defined as a focal dilation of the abdominal aorta beyond 50% of its normal diameter, is a common and potentially life-threatening vascular disease. The molecular and cellular mechanisms underlying AAA pathogenesis remain unclear. Healthy endothelial cells (ECs) play a critical role in maintaining vascular homeostasis by regulating vascular tone and maintaining an anti-inflammatory, anti-thrombotic local environment. Increasing evidence indicates that endothelial dysfunction is an early pathologic event in AAA formation, contributing to both oxidative stress and inflammation in the degenerating arterial wall. Recent studies utilizing single-cell RNA sequencing revealed heterogeneous EC sub-populations, as determined by their transcriptional profiles, in aortic aneurysm tissue. This review summarizes recent findings, including clinical evidence of endothelial dysfunction in AAA, the impact of biomechanical stress on EC in AAA, the role of endothelial nitric oxide synthase (eNOS) uncoupling in AAA, and EC heterogeneity in AAA. These studies help to improve our understanding of AAA pathogenesis and ultimately may lead to the generation of EC-targeted therapeutics to treat or prevent this deadly disease.