ArticleThe Journal of clinical investigation2014
Tgfbr2 disruption in postnatal smooth muscle impairs aortic wall homeostasis.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 1 of them a synthesis that pooled it.
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Who cites it
190 citing papers in PubMed, 1 synthesis or guideline pooled it, 285 citations in OpenAlex.
- Consideration of Sex Differences in Design and Reporting of Experimental Arterial Pathology Studies-Statement From ATVB Council.Arteriosclerosis, thrombosis, and vascular biology · 2018Guideline
- Smooth Muscle Cell Plasticity as a Central Determinant of Plaque Stability.Current atherosclerosis reports · 2026Review
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Smad3 deficiency attenuates disease severity in a zebrafish model for Smad6-related aortic disease.Angiogenesis · 2026Article
- Heritable Thoracic Aortic Diseases in Pediatric Practice: From Molecular Mechanisms to Genotype-Informed Management, a Comprehensive Narrative Review.Journal of clinical medicine · 2026Review
- Angiotensin II Induces Abdominal Aortic Branch Aneurysms inArteriosclerosis, thrombosis, and vascular biology · 2026Article
- Preclinical modeling of Loeys-Dietz syndrome: insights into mechanisms and therapy.Orphanet journal of rare diseases · 2026Review
- Mechanics and mechanobiology of arterial development.Biomechanics and modeling in mechanobiology · 2026Review
- Long-term loss of TGF-β signaling in smooth muscle cells of aged adult mice disrupts proximal aortic wall structure and homeostasis.Scientific reports · 2026Article
- A multiscale computational model of ascending thoracic aortic aneurysm development in Marfan syndrome for in silico trials.Biomechanics and modeling in mechanobiology · 2026Article
- Hydraulic fracturing-induced delamination and extravasation extends medial damage beyond the false lumen in aortic dissection.bioRxiv : the preprint server for biology · 2026Article
- SPP1BMC medicine · 2026Article
- HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells.JACC. Basic to translational science · 2026Article
- Identification of DNA methylation biomarkers in amniotic fluid for prenatal detection of congenital heart disease (CHD).Clinical epigenetics · 2026Article
- Cell-dependent contributions of thrombospondin-1 to the rupture of abdominal aortic aneurysm in mice.Cardiovascular research · 2026Article
- Functional Genomics Link REST to Endothelial Plasticity and Atherosclerosis.Circulation research · 2026Article
- Proximal aortic aneurysms in mice underexpressing transforming growth factor-β1.The journal of physiological sciences : JPS · 2025Article
- Sustained tenascin-C expression drives neointimal hyperplasia and promotes aortocaval fistula failure.American journal of physiology. Heart and circulatory physiology · 2025Article
- PIASy deficiency mitigates thoracic aortic aneurysm formation via the TGF-β/Smad2/3 pathway.Journal of thoracic disease · 2025Article
- Smooth muscle cells and fibroblasts in the ascending aorta exhibit minor differences between embryonic origins in angiotensin II-driven transcriptional alterations.Scientific reports · 2025Article
130 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
Abstract
TGF-β is essential for vascular development; however, excess TGF-β signaling promotes thoracic aortic aneurysm and dissection in multiple disorders, including Marfan syndrome. Since the pathology of TGF-β overactivity manifests primarily within the arterial media, it is widely assumed that suppression of TGF-β signaling in vascular smooth muscle cells will ameliorate aortic disease. We tested this hypothesis by conditional inactivation of Tgfbr2, which encodes the TGF-β type II receptor, in smooth muscle cells of postweanling mice. Surprisingly, the thoracic aorta rapidly thickened, dilated, and dissected in these animals. Tgfbr2 disruption predictably decreased canonical Smad signaling, but unexpectedly increased MAPK signaling. Type II receptor-independent effects of TGF-β and pathological responses by nonrecombined smooth muscle cells were excluded by serologic neutralization. Aortic disease was caused by a perturbed contractile apparatus in medial cells and growth factor production by adventitial cells, both of which resulted in maladaptive paracrine interactions between the vessel wall compartments. Treatment with rapamycin restored a quiescent smooth muscle phenotype and prevented dissection. Tgfbr2 disruption in smooth muscle cells also accelerated aneurysm growth in a murine model of Marfan syndrome. Our data indicate that basal TGF-β signaling in smooth muscle promotes postnatal aortic wall homeostasis and impedes disease progression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.