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Antioxid Redox Signal. 2020 Jan 28. doi: 10.1089/ars.2020.8035. [Epub ahead of print]

Involvement of Myeloid Cells and Non-Coding RNA in Abdominal Aortic Aneurysm Disease.

Author information

1
Klinikum rechts der Isar der Technischen Universitat Munchen, 27190, Department for Vascular and Endovascular Surgery, Ismaninger Str. 22, 81675 Munich, Munich, Germany, 81675; christoph.knappich@googlemail.com.
2
Stanford University School of Medicine, Division of Cardiovascular Medicine, Stanford, California, United States; josh.spin@gmail.com.
3
Klinikum rechts der Isar der Technischen Universitat Munchen, 27190, Department for Vascular and Endovascular Surgery, Munich, Germany; hheckstein@web.de.
4
Stanford University School of Medicine, Division of Cardiovascular Medicine, Stanford, California, United States; ptsao@stanford.edu.
5
Klinikum rechts der Isar der Technischen Universitat Munchen, 27190, Department for Vascular and Endovascular Surgery, Munich, Germany.
6
Karolinska Institute, Department of Medicine, Stockholm, Sweden; lars.maegdefessel@tum.de.

Abstract

SIGNIFICANCE:

Abdominal aortic aneurysm (AAA) is a potentially fatal condition, featuring the possibility of high-mortality rupture. To date, prophylactic surgery by means of open surgical repair (OSR) or endovascular aortic repair (EVAR) at specific thresholds are considered standard therapy. Both surgical options hold different risk profiles of short- and long-term morbidity and mortality. Targeting early stages of AAA development in order to decelerate disease progression is desirable. Recent Advances: Understanding the pathomechanisms that initiate formation, maintain growth, and promote rupture of AAA is crucial to developing new medical therapeutic options. Inflammatory cells, in particular macrophages, have been investigated for their contribution to AAA disease for decades, while evidence on lymphocytes, mast cells, and neutrophils is sparse. Recently, there has been increasing interest in non-coding RNAs (ncRNA) and their involvement in disease development, including AAA.

CRITICAL ISSUES:

The current evidence on myeloid cells and ncRNAs in AAA largely originates from small animal models, making clinical extrapolation difficult. Although it is feasible to collect surgical human AAA samples, these tissues reflect end-stage disease, preventing examination of critical mechanisms behind early AAA formation.

FUTURE DIRECTIONS:

Gaining more insight into how myeloid cells and ncRNAs contribute to AAA disease, particularly in early stages, might suggest non-surgical AAA treatment options. The utilization of large animal models might be helpful in this context to help bridge translational results to humans.

PMID:
31989839
DOI:
10.1089/ars.2020.8035

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