ReviewThe Journal of surgical research2013
Molecular mechanisms of thoracic aortic dissection.
Review in The Journal of surgical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
104 citing papers in PubMed, 227 citations in OpenAlex.
- Screening and investigating the regulatory mechanisms of oxidative stress-related biomarkers in thoracic aortic aneurysms.Journal of applied genetics · 2026Article
- The AntioxidantAntioxidants (Basel, Switzerland) · 2026Article
- Medial Neovascularization: A Novel Mechanism of Aortic Dissection in a Hypertensive Population?Journal of the American Heart Association · 2026Article
- Shape and Scale in Quantifying Aortic Morphology Evolution and Chronicity.Cardiovascular engineering and technology · 2026Article
- Proteoglycans as Biomarkers of Medial Degeneration in Acute Stanford Type A Aortic Dissection.Reviews in cardiovascular medicine · 2025Review
- Excessive glycosylation drives thoracic aortic aneurysm formation through integrated stress response.European heart journal · 2025Article
- Obesity: An Underlying Risk for Acute Aortic Dissection.Journal of clinical medicine · 2025Review
- The Involvement of Herpesviruses in the Pathogenesis of Thoracic Aortic Aneurysms: Passive Bystanders or Active Contributors?Reviews in cardiovascular medicine · 2025Review
- Loss of Myh11 K1256 Dysregulates the Extracellular Matrix and Focal Adhesion by Inhibiting Zyxin-Activated Transcription.International journal of molecular sciences · 2025Article
- CCDC80 Protects against Aortic Dissection and Rupture by Maintaining the Contractile Smooth Muscle Cell Phenotype.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Modeling Thoracic Aortic Dissection Using Patient-Specific iPSCs Reveals VSMC Dysfunction and Extracellular Matrix Dysregulation.Stem cells international · 2025Article
- Nanoparticle contrast-enhanced computed tomography of sporadic aortic aneurysm and dissection: Effect of nanoparticle size and contrast agent dose.Theranostics · 2025Article
- The prognostic impact of maximal aortic diameter on acute type B aortic dissection progression in a Chinese population.Scientific reports · 2024Article
- Expression ofExperimental and therapeutic medicine · 2024Article
- Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization.Cardiovascular diabetology · 2024Article
- TheFrontiers in cardiovascular medicine · 2024Article
- Association of polymorphisms inOpen medicine (Warsaw, Poland) · 2024Article
- Article
- Tomo-seq identifies NINJ1 as a potential target for anti-inflammatory strategy in thoracic aortic dissection.BMC medicine · 2023Article
- Causal Role for Neutrophil Elastase in Thoracic Aortic Dissection in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
44 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Thoracic aortic dissection (TAD) is a highly lethal vascular disease. In many patients with TAD, the aorta progressively dilates and ultimately ruptures. Dissection formation, progression, and rupture cannot be reliably prevented pharmacologically because the molecular mechanisms of aortic wall degeneration are poorly understood. The key histopathologic feature of TAD is medial degeneration, a process characterized by smooth muscle cell depletion and extracellular matrix degradation. These structural changes have a profound impact on the functional properties of the aortic wall and can result from excessive protease-mediated destruction of the extracellular matrix, altered signaling pathways, and altered gene expression. Review of the literature reveals differences in the processes that lead to ascending versus descending and sporadic versus hereditary TAD. These differences add to the complexity of this disease. Although tremendous progress has been made in diagnosing and treating TAD, a better understanding of the molecular, cellular, and genetic mechanisms that cause this disease is necessary to developing more effective preventative and therapeutic treatment strategies.
Indexed as
Identifiers
What OpenQuestion holds
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.