ResearchIn-Press PreviewVascular biology
Open Access | 10.1172/jci.insight.141673
1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
Find articles by Zhao, G. in: JCI | PubMed | Google Scholar
1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Chang, Z.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Zhao, Y.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Guo, Y.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Lu, H.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Liang, W.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Rom, O.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Wang, H.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Fan, Y.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Chen, E.
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1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, United States of America
2Department of Cell Biology, University of Cincinnati College of Medicine, Cincinnati, United States of America
3Department of Cardiac Surgery, University of Michigan Medical Center, Ann Arbor, United States of America
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Zhang, J.
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Published January 28, 2021 - More info
Abdominal aortic aneurysm (AAA) is a life-threatening degenerative vascular disease. Endothelial cell (EC) dysfunction is implicated in AAA. Our group recently demonstrated that Krüppel-like factor 11 (KLF11) plays an essential role in maintaining vascular homeostasis, at least partially through inhibition of EC inflammatory activation. However, the functions of endothelial KLF11 in AAA remain unknown. Here we found that endothelial KLF11 expression was reduced in the ECs from human aneurysms and was time-dependently decreased in the aneurysmal endothelium from both elastase- and Pcsk9/AngII-induced AAA mouse models. KLF11 deficiency in ECs markedly aggravated AAA formation, whereas EC-selective KLF11 overexpression significantly inhibited AAA formation. Mechanistically, KLF11 not only inhibited the EC inflammatory response but also diminished MMP9 expression and activity and reduced NADPH oxidase 2-mediated production of reactive oxygen species in ECs. In addition, KLF11-deficient ECs induce smooth muscle cell dedifferentiation and apoptosis. Overall, we established endothelial KLF11 as a novel factor protecting against AAA and a potential target for intervention in aortic aneurysms.