Endoplasmic reticulum stress and mitochondrial biogenesis are potential therapeutic targets for abdominal aortic aneurysm

被引:12
|
作者
Miyao, Masashi [1 ,2 ]
Cicalese, Stephanie [1 ]
Cooper, Hannah A. [1 ]
Eguchi, Satoru [1 ]
机构
[1] Temple Univ, Lewis Katz Sch Med, Cardiovasc Res Ctr, 3500 N Broad St, Philadelphia, PA 19140 USA
[2] Kyoto Univ, Grad Sch Med, Dept Forens Med, Sakyo Ku, Yoshida Konoe Cho, Kyoto 6068501, Japan
关键词
UNFOLDED PROTEIN RESPONSE; ANGIOTENSIN-II; APOPTOSIS; 7-KETOCHOLESTEROL; MODEL; DEFICIENCY; MECHANISMS; FAMILY; ER;
D O I
10.1042/CS20190648
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Endoplasmic reticulum (ER) and mitochondria are crucial organelles for cell homeostasis and alterations of these organelles have been implicated in cardiovascular disease. However, their roles in abdominal aortic aneurysm (AAA) pathogenesis remain largely unknown. In a recent issue of Clinical Science, Navas-Madronal et al. ((2019), 133(13), 1421-1438) reported that enhanced ER stress and dysregulation of mitochondrial biogenesis are associated with AAA pathogenesis in humans. The authors also proposed that disruption in oxysterols network such as an elevated concentration of 7-ketocholestyerol in plasma is a causative factor for AAA progression. Their findings highlight new insights into the underlying mechanism of AAA progression through ER stress and dysregulation of mitochondrial biogenesis. Here, we will discuss the background, significance of the study, and future directions.
引用
收藏
页码:2023 / 2028
页数:6
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