ArticleThe Journal of clinical investigation2020
Proliferative, degradative smooth muscle cells promote aortic disease.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Advanced technologies of artery-on-a-chip: a review of construction strategies and disease models.Angiogenesis · 2026Review
- Aortic dissection as a disease of vascular wall homeostasis: integrating vasa vasorum-inflammation-metabolism axis for mechanistic insight and clinical translation.Frontiers in immunology · 2026Review
- Chronic Edema Associated with Cor Pulmonale in Cattle.Animals : an open access journal from MDPI · 2025Article
- TRPM7 channel activity promotes the pathogenesis of abdominal aortic aneurysms.Nature cardiovascular research · 2025Article
- NCOR1 maintains the homeostasis of vascular smooth muscle cells and protects against aortic aneurysm.Cell death and differentiation · 2023Article
- Single-Cell RNA-Seq Reveals a Population of Smooth Muscle Cells Responsible for Atherogenesis.Aging and disease · 2022Article
- Human Umbilical Cord Mesenchymal Stem Cells Attenuate Abdominal Aortic Aneurysm Progression in Sprague-Dawley Rats: Implication of Vascular Smooth Muscle Cell Phenotypic Modulation.Stem cells and development · 2020Article
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2 authors at 2 institutions in 2 countries.
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Abstract
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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Registered trials
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