ArticleEBioMedicine2017
A Functional Variant of SMAD4 Enhances Thoracic Aortic Aneurysm and Dissection Risk through Promoting Smooth Muscle Cell Apoptosis and Proteoglycan Degradation.
Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- TRIM9-Mediated Degradation of SMAD4 Promotes Pyroptosis and Disruption of the Endothelial Barrier in Aortic Dissection Disease.Cardiovascular toxicology · 2026Article
- Mothers against decapentaplegic homolog 4 as a proteomic hub in vascular remodeling and residual cardiovascular risk.World journal of cardiology · 2026Article
- Proteoglycans as Biomarkers of Medial Degeneration in Acute Stanford Type A Aortic Dissection.Reviews in cardiovascular medicine · 2025Review
- Role of elastic fiber degradation in disease pathogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2023Review
- Role of non-coding variants in cardiovascular disease.Journal of cellular and molecular medicine · 2023Review
- Extracellular Vesicles from miR-148a-5p-Enriched Bone Marrow Mesenchymal Stem Cells Relieve Hepatic Fibrosis by Targeting Smad4.Molecular biotechnology · 2022Article
- LncRNA H19 Regulates Proliferation, Apoptosis and ECM Degradation of Aortic Smooth Muscle Cells Via miR-1-3p/ADAM10 Axis in Thoracic Aortic Aneurysm.Biochemical genetics · 2022Article
- The role of vascular smooth muscle cells in the development of aortic aneurysms and dissections.European journal of clinical investigation · 2022Review
- SMAD4 rs10502913 is Significantly Associated with Chronic Obstructive Pulmonary Disease in a Chinese Han Population: A Case-Control Study.International journal of chronic obstructive pulmonary disease · 2022Article
- Applying multi-omics techniques to the discovery of biomarkers for acute aortic dissection.Frontiers in cardiovascular medicine · 2022Review
- Moderate aerobic exercise prevents matrix degradation and death in a mouse model of aortic dissection and aneurysm.American journal of physiology. Heart and circulatory physiology · 2021Article
- Transcriptome and N6-Methyladenosine RNA Methylome Analyses in Aortic Dissection and Normal Human Aorta.Frontiers in cardiovascular medicine · 2021Article
- Circular RNA circDUS2 Is a Potential Biomarker for Intracranial Aneurysm.Frontiers in aging neuroscience · 2021Article
- Association ofFrontiers in cardiovascular medicine · 2021Article
- The Role of Inflammation and Myeloperoxidase-Related Oxidative Stress in the Pathogenesis of Genetically Triggered Thoracic Aortic Aneurysms.International journal of molecular sciences · 2020Review
- Novel Alternatively Spliced Variants of Smad4 Expressed in TGF-β-Induced EMT Regulating Proliferation and Migration of A549 Cells.OncoTargets and therapy · 2020Article
- A functional variant ofAging · 2018Article
- A role for proteoglycans in vascular disease.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Genetic variants in mRNA untranslated regions.Wiley interdisciplinary reviews. RNA · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies indicate important roles for SMAD4 in SMCs proliferation, extracellular matrix maintenance, and blood vessel remodeling. However, the genetic effects of SMAD4 in the pathogenesis of thoracic aortic aneurysm and dissection (TAAD) are still largely unknown. Here we identified a functional variant of SMAD4 which might be involved in the pathological progression of TAAD. Five tagging SNPs of SMAD4 were genotyped in 202 TAAD cases and 400 controls using MALDI-TOF. rs12455792 CT or TT variant genotypes was associated with an significantly elevated TAAD risk (adjusted OR=1.58, 95%CI=1.09-2.30) under a dominant genetic model. It was located in the 5'UTR and predicted to influence transcription activity and RNA folding of SMAD4. In luciferase reporter assay, rs12455792 T allele markedly decreased luciferase activities. Accordingly, SMAD4 expression in tissues was lower in patients with CT or TT genotypes, compared with CC. Movat's pentachrome showed that rs12455792 T allele enhanced SMCs loss and fibers accumulation. With angiotensin II induction, rate of Apoptotic SMCs was significantly higher while SMAD4 silenced. Moreover, rs12455792 T allele also increased Versican degradation via ADAMTS-4. In conclusion, this variant might promote SMCs apoptosis and proteoglycans degradation, and further facilitate the progress of TAAD. Our findings identified rs12455792 as a predictor for progression of vascular media pathological changes related thoracic aortic disorders.
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.