The putative role of autophagy in the pathogenesis of abdominal aortic aneurysms. (February 2017)

• Record Type: Journal Article
• Authors: Ramadan, Azza; Al-Omran, Mohammed; Verma, Subodh
• Is Part Of: Atherosclerosis. Volume 257(2017)
• Page Start: 288
• Page End: 296
• Publication Date: 2017-02
• Subjects: Abdominal aortic aneurysm -- Autophagy -- Macrophages -- Smooth muscle cells -- Endothelial cells; Arteriosclerosis -- Periodicals; Electronic journals; 616.136
• DOI: 10.1016/j.atherosclerosis.2017.01.017
• Languages: English
• ISSNs: 0021-9150

Abstract

Abstract: Abdominal aortic aneurysms (AAA) are a significant cause of worldwide mortality and morbidity. While the histopathological characteristics of AAA are well documented, the cellular and molecular mechanisms involved in the pathogenesis of AAA are not entirely understood. Autophagy is a highly conserved basal cellular process in eukaryotic cells that involves the turnover of organelles and proteins. It is also activated as an adaptive response to stressful conditions to promote cell survival. While autophagy typically promotes pro-survival processes, it can sometimes lead to cellular demise. Preclinical studies have revealed autophagy to be a protective mechanism in certain vascular diseases with several autophagy-related genes reported to be markedly upregulated in human aneurysmal tissue. The role autophagy plays in the pathogenesis of AAA, however, remains poorly defined. In this review, we discuss the putative role of autophagy in AAA by reviewing several in vitro and in vivo studies that address the functional significance of autophagy in cells that are involved in the pathophysiology of AAA, amongst which are macrophages, smooth muscle and endothelial cells. Highlights: Multiple autophagy-related genes are upregulated in human abdominal aortic aneurysms (AAA). Several AAA-related factors are autophagy inducers. Loss of macrophage and smooth muscle autophagy could exacerbate AAA. Endothelial autophagy may have a dual role in AAA pathogenesis.