Proliferative, degradative smooth muscle cells promote aortic disease
Maarten Hulsmans1 and Matthias Nahrendorf1,2,3
1Center for Systems Biology, Department of Radiology, and
2Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
3Department of Internal Medicine I, University Hospital Würzburg, Würzburg, Germany.
Address correspondence to: Matthias Nahrendorf, Simches Research Building, Room 8-226, 185 Cambridge Street, Boston, Massachusetts 02114, USA. Phone: 617.724.6242; Email: mnahrendorf@mgh.harvard.edu.
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1Center for Systems Biology, Department of Radiology, and
2Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.
3Department of Internal Medicine I, University Hospital Würzburg, Würzburg, Germany.
Address correspondence to: Matthias Nahrendorf, Simches Research Building, Room 8-226, 185 Cambridge Street, Boston, Massachusetts 02114, USA. Phone: 617.724.6242; Email: mnahrendorf@mgh.harvard.edu.
Find articles by Nahrendorf, M. in: JCI | PubMed | Google Scholar
First published February 10, 2020 - More info
J Clin Invest. 2020;130(3):1096–1098. https://doi.org/10.1172/JCI134019.
© 2020 American Society for Clinical Investigation
Aneurysms are common in the abdominal and thoracic regions of the aorta and can cause death due to dissection or rupture. Traditionally, thoracic aortic aneurysms have been labeled as a degenerative disease, characterized by alterations in extracellular matrix and loss of smooth muscle cells (SMCs) in the medial layer of the aortic wall. In this issue of the JCI, Li and colleagues introduce an unconventional concept by demonstrating that mTOR-dependent proliferative SMCs render the aortic wall vulnerable to dilatation and dissection rather than prevent disease progression. These vascular SMCs, termed degradative SMCs, compromise the medial properties and function of the aortic wall by enhanced proteolytic and phagocytic activity; however, the cells do not transdifferentiate into macrophages. The degradative SMC phenotype also worsens atherosclerotic disease and could thus be considered as a therapeutic target for diverse aortic diseases.
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