ArticleAging2019
TGF-β mediates aortic smooth muscle cell senescence in Marfan syndrome.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 51 citations in OpenAlex.
- Article
- Development of a zebrafish model of Loeys-Dietz syndrome through tgfbr2b knockdown.Journal of human genetics · 2026Article
- Oxidative Stress-Induced DNA Damage Response Pathways in Aortic Disease: Implications for Inflammation and Vascular Degeneration.International journal of molecular sciences · 2026Review
- Integration of Multi-Omics and Machine Learning Identifies TGFB1 and SERPINE1 as Biomarkers of Vascular Smooth Muscle Cell Senescence in Intracranial Aneurysms.Translational stroke research · 2026Article
- Arterial origin-dependent susceptibility of vascular smooth muscle cells to prelamin A-induced senescence and rescue by umbilical artery-derived decellularized extracellular matrix.International journal of clinical and experimental pathology · 2026Article
- Endothelial Cell Senescence in Marfan Syndrome: Pathogenesis and Therapeutic Potential of TGF-β Pathway Inhibition.Journal of the American Heart Association · 2025Article
- Single-Cell Transcriptomic Reveals the Involvement of Cell-Cell Junctions in the Early Development of Hypertrophic Cardiomyopathy.Journal of cellular and molecular medicine · 2025Article
- Therapeutic Opportunities of Marfan Syndrome: Current Perspectives.Drug design, development and therapy · 2025Review
- Greater TIMP-1 protein levels and neointimal formation represent sex-dependent cellular events limiting aortic vessel expansion in female rats.IUBMB life · 2024Article
- Ciprofloxacin Accelerates Angiotensin-II-Induced Vascular Smooth Muscle Cells Senescence Through Modulating AMPK/ROS pathway in Aortic Aneurysm and Dissection.Cardiovascular toxicology · 2024Article
- Roles and Mechanisms of miRNAs in Abdominal Aortic Aneurysm: Signaling Pathways and Clinical Insights.Current atherosclerosis reports · 2024Review
- Increased vascular smooth muscle cell senescence in aneurysmal Fibulin-4 mutant mice.npj aging · 2024Article
- Unveiling cellular and molecular aspects of ascending thoracic aortic aneurysms and dissections.Basic research in cardiology · 2024Review
- Senescence-Associated Alterations in Matrisome of Mesenchymal Stem Cells.International journal of molecular sciences · 2024Article
- Transcriptome analysis reveals therapeutic potential of NAMPT in protecting against abdominal aortic aneurysm in human and mouse.Bioactive materials · 2024Article
- Regnase-1 overexpression as a therapeutic approach of Marfan syndrome.Molecular therapy. Methods & clinical development · 2024Article
- Connecting epigenetics and inflammation in vascular senescence: state of the art, biomarkers and senotherapeutics.Frontiers in genetics · 2024Review
- Targeting Vascular Smooth Muscle Cell Senescence: A Novel Strategy for Vascular Diseases.Journal of cardiovascular translational research · 2023Review
- Redox Dysregulation of Vascular Smooth Muscle Sirtuin-1 in Thoracic Aortic Aneurysm in Marfan Syndrome.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- MicroRNA-19b-3p dysfunction of mesenchymal stem cell-derived exosomes from patients with abdominal aortic aneurysm impairs therapeutic efficacy.Journal of nanobiotechnology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Formation of aortic aneurysms as a consequence of augmented transforming growth factor β (TGF-β) signaling and vascular smooth muscle cell (VSMC) dysfunction is a potentially lethal complication of Marfan syndrome (MFS). Here, we examined VSMC senescence in patients with MFS and explored the potential mechanisms that link VSMC senescence and TGF-β. Tissue was harvested from the ascending aorta of control donors and MFS patients, and VSMCs were isolated. Senescence-associated β-galactosidase (SA-β-gal) activity and expression of senescence-related proteins (p53, p21) were significantly higher in aneurysmal tissue from MFS patients than in healthy aortic tissue from control donors. Compared to control-VSMCs, MFS-VSMCs were larger with higher levels of both SA-β-gal activity and mitochondrial reactive oxygen species (ROS). In addition, TGF-β1 levels were much higher in MFS- than control-VSMCs. TGF-β1 induced VSMC senescence through excessive ROS generation. This effect was suppressed by Mito-tempo, a mitochondria-targeted antioxidant, or SC-514, a NF-κB inhibitor. This suggests TGF-β1 induces VSMC senescence through ROS-mediated activation of NF-κB signaling. It thus appears that a TGF-β1/ROS/NF-κB axis may mediate VSMC senescence and aneurysm formation in MFS patients. This finding could serve as the basis for a novel strategy for treating aortic aneurysm in MFS.
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Registered trials
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.