ArticleJournal of the American Heart Association2015
Loss of the mechanotransducer zyxin promotes a synthetic phenotype of vascular smooth muscle cells.
Article in Journal of the American Heart Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Extreme Diversity of the Human Vascular Mesenchymal Cell Landscape.Journal of the American Heart Association · 2020Pooled it
- Complement Anaphylatoxin C5a-Induced Mouse Lymphatic Functions Modulate Interactions Between Endothelial Cells and T Lymphocytes.Immune network · 2026Article
- Focal Adhesion and Cancer Cell Cycle-Associated Resistance.ACS omega · 2026Review
- The Potential Link and Role of Zyxin in the Pathogenesis of Psoriasis and Its Associated Comorbidities.International journal of molecular sciences · 2026Article
- Loss of Myh11 K1256 Dysregulates the Extracellular Matrix and Focal Adhesion by Inhibiting Zyxin-Activated Transcription.International journal of molecular sciences · 2025Article
- C/EBPβ-Lin28a positive feedback loop triggered by C/EBPβ hypomethylation enhances the proliferation and migration of vascular smooth muscle cells in restenosis.Chinese medical journal · 2025Article
- TBK1-Zyxin signaling controls tumor-associated macrophage recruitment to mitigate antitumor immunity.The EMBO journal · 2024Article
- Principles and regulation of mechanosensing.Journal of cell science · 2024Review
- Stress, Vascular Smooth Muscle Cell Phenotype and Atherosclerosis: Novel Insight into Smooth Muscle Cell Phenotypic Transition in Atherosclerosis.Current atherosclerosis reports · 2024Review
- Zyxin is important for the stability and function of podocytes, especially during mechanical stretch.Communications biology · 2024Article
- Characterisation of Lipoma-Preferred Partner as a Novel Mechanotransducer in Vascular Smooth Muscle Cells.Cells · 2023Article
- Quantitative proteomic analysis of human serum using tandem mass tags to predict cardiovascular risks in patients with psoriasis.Scientific reports · 2023Article
- Expression of Zyxin in Non-Small Cell Lung Cancer-A Preliminary Study.Biomolecules · 2022Article
- Review
- Zyxin protects from hypertension-induced cardiac dysfunction.Cellular and molecular life sciences : CMLS · 2022Article
- Analysis of 200,000 Exome-Sequenced UK Biobank Subjects Implicates Genes Involved in Increased and Decreased Risk of Hypertension.Pulse (Basel, Switzerland) · 2021Article
- Review
- Review
- Lin11-Isl1-Mec3 Domain Proteins as Mechanotransducers in Endothelial and Vascular Smooth Muscle Cells.Frontiers in physiology · 2021Review
- Loss of the serine protease HTRA1 impairs smooth muscle cells maturation.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExposure of vascular smooth muscle cells (VSMCs) to excessive cyclic stretch such as in hypertension causes a shift in their phenotype. The focal adhesion protein zyxin can transduce such biomechanical stimuli to the nucleus of both endothelial cells and VSMCs, albeit with different thresholds and kinetics. However, there is no distinct vascular phenotype in young zyxin-deficient mice, possibly due to functional redundancy among other gene products belonging to the zyxin family. Analyzing zyxin function in VSMCs at the cellular level might thus offer a better mechanistic insight. We aimed to characterize zyxin-dependent changes in gene expression in VSMCs exposed to biomechanical stretch and define the functional role of zyxin in controlling the resultant VSMC phenotype. METHODS AND
resultsDNA microarray analysis was used to identify genes and pathways that were zyxin regulated in static and stretched human umbilical artery-derived and mouse aortic VSMCs. Zyxin-null VSMCs showed a remarkable shift to a growth-promoting, less apoptotic, promigratory and poorly contractile phenotype with ≈90% of the stretch-responsive genes being zyxin dependent. Interestingly, zyxin-null cells already seemed primed for such a synthetic phenotype, with mechanical stretch further accentuating it. This could be accounted for by higher RhoA activity and myocardin-related transcription factor-A mainly localized to the nucleus of zyxin-null VSMCs, and a condensed and localized accumulation of F-actin upon stretch.
conclusionsAt the cellular level, zyxin is a key regulator of stretch-induced gene expression. Loss of zyxin drives VSMCs toward a synthetic phenotype, a process further consolidated by exaggerated stretch.
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