ReviewArteriosclerosis, thrombosis, and vascular biology2017
Altered Smooth Muscle Cell Force Generation as a Driver of Thoracic Aortic Aneurysms and Dissections.
Review in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 154 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
154 citing papers in PubMed, 246 citations in OpenAlex.
- Mouse Models of Aortic Pathologies: Deciphering Molecular and Cellular Mechanisms from Bench to Bedside.CJC open · 2026Review
- ADAR1 and ADAR2 Expression in the Thoracic Aortic Wall Correlates with Aneurysm Severity and Dissection Risk: Insights into A-to-I RNA Editing Dysregulation in Marfan Syndrome-Derived vSMCs.International journal of molecular sciences · 2026Article
- Vascular Smooth Muscle Myosin 2 Filaments Dynamically Assemble and Stabilize During Induced Contractility.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Phenotypic modulation of corpus cavernosum smooth muscle cells in type 2 diabetic rats is mediated by regulated exosomes secretion via neutral sphingomyelinase-2.Asian journal of andrology · 2026Article
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Heritable Thoracic Aortic Diseases in Pediatric Practice: From Molecular Mechanisms to Genotype-Informed Management, a Comprehensive Narrative Review.Journal of clinical medicine · 2026Review
- Mechanotransduction in Marfan Syndrome and Related Aortic Disorders: Insights from Transcriptomic Analyses.Genes · 2026Review
- Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease.Cells · 2026Review
- Focal adhesion proteins confer smooth muscle anoikis resistance and protection against aortic aneurysm and dissection.JCI insight · 2026Article
- Exercise Attenuates Aortic Dissection Via PDE5A-Mediated Inhibition of Vascular Smooth Muscle Cell Phenotypic Switch.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Vascular Smooth Muscle Myosin 2 Filaments Dynamically Assemble and Stabilize During Induced Contractility.bioRxiv : the preprint server for biology · 2026Article
- Structural and transcriptomic alterations underlying the progression of aortic dissection in Fbn1Scientific reports · 2026Article
- MYH11 variants in thoracic aortic aneurysm pathophysiology: From bench to bedside.European journal of clinical investigation · 2026Review
- Article
- Article
- 2025 report on advances in thoracic aortic disease research.Journal of thoracic disease · 2026Review
- Case Report: Diagnostic odyssey in rare diseases: when genetic variants are misinterpreted.Frontiers in pediatrics · 2026Article
- Genetic Causes of Thoracic Aortic Aneurysm: A Review.Methodist DeBakey cardiovascular journal · 2026Review
- Calcium channel blockers increase the risk of aortic aneurysm and dissection.Nature communications · 2025Article
- The transcription factor RBPJ is required for inflammatory macrophage activation in thoracic aortic dissection by mediating mechanotransduction-induced glycolysis.Cellular and molecular life sciences : CMLS · 2025Article
94 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedCorrection.2017
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The importance of maintaining contractile function in aortic smooth muscle cells (SMCs) is evident by the fact that heterozygous mutations in the major structural proteins or kinases controlling contraction lead to the formation of aneurysms of the ascending thoracic aorta that predispose to life-threatening aortic dissections. Force generation by SMC requires ATP-dependent cyclic interactions between filaments composed of SMC-specific isoforms of α-actin (encoded by ACTA2) and myosin heavy chain (MYH11). ACTA2 and MYH11 mutations are predicted or have been shown to disrupt this cyclic interaction predispose to thoracic aortic disease. Movement of the myosin motor domain is controlled by phosphorylation of the regulatory light chain on the myosin filament, and loss-of-function mutations in the dedicated kinase for this phosphorylation, myosin light chain kinase (MYLK) also predispose to thoracic aortic disease. Finally, a mutation in the cGMP-activated protein kinase (PRKG1) results in constitutive activation of the kinase in the absence of cGMP, thus driving SMC relaxation in part through increased dephosphorylation of the regulatory light chain and predisposes to thoracic aortic disease. Furthermore, SMCs cannot generate force without connections to the extracellular matrix through focal adhesions, and mutations in the major protein in the extracellular matrix, fibrillin-1, linking SMCs to the matrix also cause thoracic aortic disease in individuals with Marfan syndrome. Thus, disruption of the ability of the aortic SMC to generate force through the elastin-contractile units in response to pulsatile blood flow may be a primary driver for thoracic aortic aneurysms and dissections.
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.