ArticleThe Journal of biological chemistry2014
Overexpression of smooth muscle myosin heavy chain leads to activation of the unfolded protein response and autophagic turnover of thick filament-associated proteins in vascular smooth muscle cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- The diagnostic value of D-dimer in acute aortic dissection: a meta-analysis.Journal of cardiothoracic surgery · 2021Pooled it
- Targeted Sequencing of Human Aorta Tissue Reveals Undiagnosed Heritable Thoracic Aortic Disease.Interdisciplinary cardiovascular and thoracic surgery · 2026Article
- MYH11 variants in thoracic aortic aneurysm pathophysiology: From bench to bedside.European journal of clinical investigation · 2026Review
- MAPK14 converges on key transcriptional machinery to promote vascular smooth muscle cell degeneration in abdominal aortic aneurysm.Signal transduction and targeted therapy · 2026Article
- How Can Molecules Induce Hemorrhoids? The Role of Genetics and Epigenetics in Hemorrhoidal Disease.International journal of molecular sciences · 2025Review
- Interpreting MYH11 Copy Number Variation in Thoracic Aortic Aneurysm and Dissection: Insights From the Misannotation of Variants in Clinical Genetic Tests.JACC. Case reports · 2025Article
- Comprehensive identification of hub mRNAs and lncRNAs in colorectal cancer using galaxy: an in silico transcriptome analysis.Discover oncology · 2025Article
- Dimethyl Fumarate Mediates Sustained Vascular Smooth Muscle Cell Remodeling in a Mouse Model of Cerebral Aneurysm.Antioxidants (Basel, Switzerland) · 2024Article
- Proteomic and functional characterization of intra-tumor heterogeneity in human endometrial cancer.Cell reports. Medicine · 2022Article
- An Myh11 single lysine deletion causes aortic dissection by reducing aortic structural integrity and contractility.Scientific reports · 2022Article
- Molecular phenotyping and functional assessment of smooth muscle-like cells with pathogenic variants in aneurysm genes ACTA2, MYH11, SMAD3 and FBN1.Human molecular genetics · 2021Article
- Article
- Proteomics study on the effect of silybin on cardiomyopathy in obese mice.Scientific reports · 2021Article
- Article
- The molecular mechanism of induction of unfolded protein response by Chlamydia.Biochemical and biophysical research communications · 2019Article
- TMCO1 is essential for ovarian follicle development by regulating ER CaCell death and differentiation · 2018Article
- Familial aortic disease and a large duplication in chromosome 16p13.1.Molecular genetics & genomic medicine · 2018Article
- EZH2 inhibits autophagic cell death of aortic vascular smooth muscle cells to affect aortic dissection.Cell death & disease · 2018Article
- Molecular pathogenesis of genetic and sporadic aortic aneurysms and dissections.Current problems in surgery · 2017Review
- Altered Smooth Muscle Cell Force Generation as a Driver of Thoracic Aortic Aneurysms and Dissections.Arteriosclerosis, thrombosis, and vascular biology · 2017Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Duplications spanning nine genes at the genomic locus 16p13.1 predispose individuals to acute aortic dissections. The most likely candidate gene in this region leading to the predisposition for dissection is MYH11, which encodes smooth muscle myosin heavy chain (SM-MHC). The effects of increased expression of MYH11 on smooth muscle cell (SMC) phenotypes were explored using mouse aortic SMCs with transgenic overexpression of one isoform of SM-MHC. We found that these cells show increased expression of Myh11 and myosin filament-associated contractile genes at the message level when compared with control SMCs, but not at the protein level due to increased protein degradation. Increased expression of Myh11 resulted in endoplasmic reticulum (ER) stress in SMCs, which led to a paradoxical decrease of protein levels through increased autophagic degradation. An additional consequence of ER stress in SMCs was increased intracellular calcium ion concentration, resulting in increased contractile signaling and contraction. The increased signals for contraction further promote transcription of contractile genes, leading to a feedback loop of metabolic abnormalities in these SMCs. We suggest that overexpression of MYH11 can lead to increased ER stress and autophagy, findings that may be globally implicated in disease processes associated with genomic duplications.
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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.