ArticleJournal of the American Heart Association2014
Arterial wall stress controls NFAT5 activity in vascular smooth muscle cells.
Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 49 citations in OpenAlex.
- Distinct molecular profiles in human aortic smooth muscle cells under cyclic stretch and hydrostatic pressure.The journal of physiological sciences : JPS · 2026Article
- Deciphering the Tenascin-C Nexus: A Comprehensive Review of Its Involvement in Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Review
- Multidimensional excavation of the current status and trends of mechanobiology in cardiovascular homeostasis and remodeling within 20 years.Mechanobiology in medicine · 2025Review
- Adequate post-ischemic reperfusion of the mouse brain requires endothelial NFAT5.Acta neuropathologica communications · 2024Article
- Essential Roles of PIEZO1 in Mammalian Cardiovascular System: From Development to Diseases.Cells · 2024Review
- Sodium, Interstitium, Lymphatics and Hypertension-A Tale of Hydraulics.Hypertension (Dallas, Tex. : 1979) · 2024Review
- Biology of Tenascin C and its Role in Physiology and Pathology.Current medicinal chemistry · 2024Review
- When Phased without Water: Biophysics of Cellular Desiccation, from Biomolecules to Condensates.Chemical reviews · 2023Review
- Hypothalamic Oxytocin Neuron Activation Attenuates Intermittent Hypoxia-Induced Hypertension and Cardiac Dysfunction in an Animal Model of Sleep Apnea.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Review
- Article
- NFAT5-Mediated Signalling Pathways in Viral Infection and Cardiovascular Dysfunction.International journal of molecular sciences · 2021Review
- Review
- Actin Beta-Like 2 as a New Mediator of Proliferation and Migration in Epithelial Ovarian Cancer.Frontiers in oncology · 2021Article
- Article
- Biomechanical signal communication in vascular smooth muscle cells.Journal of cell communication and signaling · 2020Review
- Tissue sodium excess is not hypertonic and reflects extracellular volume expansion.Nature communications · 2020Article
- Co-expression of glycosylated aquaporin-1 and transcription factor NFAT5 contributes to aortic stiffness in diabetic and atherosclerosis-prone mice.Journal of cellular and molecular medicine · 2020Article
- Circulating miR-206 and Wnt-signaling are associated with cardiovascular complications and a history of preeclampsia in women.Clinical science (London, England : 1979) · 2020Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNuclear factor of activated T-cells 5 (NFAT5) has recently been described to control the phenotype of vascular smooth muscle cells (VSMCs). Although an increase in wall stress or stretch (eg, elicited by hypertension) is a prototypic determinant of VSMC activation, the impact of this biomechanical force on the activity of NFAT5 is unknown. This study intended to reveal the function of NFAT5 and to explore potential signal transduction pathways leading to its activation in stretch-stimulated VSMCs. METHODS AND
resultsHuman arterial VSMCs were exposed to biomechanical stretch and subjected to immunofluorescence and protein-biochemical analyses. Stretch promoted the translocation of NFAT5 to the nucleus within 24 hours. While the protein abundance of NFAT5 was regulated through activation of c-Jun N-terminal kinase under these conditions, its translocation required prior activation of palmitoyltransferases. DNA microarray and ChiP analyses identified the matrix molecule tenascin-C as a prominent transcriptional target of NFAT5 under these conditions that stimulates migration of VSMCs. Analyses of isolated mouse femoral arteries exposed to hypertensive perfusion conditions verified that NFAT5 translocation to the nucleus is followed by an increase in tenascin-C abundance in the vessel wall.
conclusionsCollectively, our data suggest that biomechanical stretch is sufficient to activate NFAT5 both in native and cultured VSMCs where it regulates the expression of tenascin-C. This may contribute to an improved migratory activity of VSMCs and thus promote maladaptive vascular remodeling processes such as hypertension-induced arterial stiffening.
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.