ArticleiScience2020
YAP/TAZ Are Required to Suppress Osteogenic Differentiation of Vascular Smooth Muscle Cells.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 45 citations in OpenAlex.
- Novel insights into the role of the renal interstitial microenvironment in Randall's plaque formation (Review).International journal of molecular medicine · 2026Review
- Macrophage-MSCs Interplay in Orthodontic Bone Remodelling: Mechanics-Immunity-Stem Cell Axis.International dental journal · 2026Review
- Caffeic acid phenethyl ester ameliorates high-fat diet-induced muscle textural deterioration in grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Uric acid-associated mechanisms of coronary artery calcification in diabetic kidney disease: evidence, hypotheses, and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
- Spatial architecture of atherosclerotic plaques: coordinating immune responses through mechanotransduction and vesicular trafficking.Frontiers in cell and developmental biology · 2026Review
- YAP/TAZ deletion in vascular smooth muscle cells mirrors atherosclerosis-associated transcriptional programs.Journal of molecular and cellular cardiology plus · 2025Article
- Orphan receptor GPR153 facilitates vascular damage responses by modulating cAMP levels, YAP/TAZ signaling, and NF-κB activation.Nature communications · 2025Article
- Hippo in smooth muscle - a therapeutic target in vascular diseases driven by aging and hypertension.Frontiers in physiology · 2025Review
- Vascular smooth muscle cells can be circumferentially aligned inside a channel using tunable gelatin microribbons.Biofabrication · 2024Article
- Review
- The Role of NOTCH Pathway Genes in the Inherited Susceptibility to Aortic Stenosis.Journal of cardiovascular development and disease · 2024Article
- Mir-195-5p targets Smad7 regulation of the Wnt/β-catenin pathway to promote osteogenic differentiation of vascular smooth muscle cells.BMC cardiovascular disorders · 2024Article
- Dynamic Hippo pathway activity underlies mesenchymal differentiation during lung alveolar morphogenesis.Development (Cambridge, England) · 2024Article
- Vascular smooth muscle-specific YAP/TAZ deletion triggers aneurysm development in mouse aorta.JCI insight · 2023Article
- Yes-Associated Protein and Transcriptional Coactivator with PDZ-Binding Motif in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- The Hippo signalling pathway and its implications in human health and diseases.Signal transduction and targeted therapy · 2022Review
- Mechanisms of pulmonary vascular dysfunction in pulmonary hypertension and implications for novel therapies.American journal of physiology. Heart and circulatory physiology · 2022Review
- New Therapeutics Targeting Arterial Media Calcification: Friend or Foe for Bone Mineralization?Metabolites · 2022Review
- YAP and TAZ in Vascular Smooth Muscle Confer Protection Against Hypertensive Vasculopathy.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Vascular smooth muscle cells in intimal hyperplasia, an update.Frontiers in physiology · 2022Review
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular smooth muscle cells (VSMCs) represent the prevailing cell type of arterial vessels and are essential for blood vessel structure and homeostasis. They have substantial potential for phenotypic plasticity when exposed to various stimuli in their local microenvironment. How VSMCs maintain their differentiated contractile phenotype is still poorly understood. Here we demonstrate that the Hippo pathway effectors YAP and TAZ play a critical role in maintaining the differentiated contractile phenotype of VSMCs. In the absence of YAP/TAZ, VSMCs lose their differentiated phenotype and undergo osteogenic differentiation, which results in vascular calcification. Osteogenic transdifferentiation was accompanied by the upregulation of Wnt target genes. The absence of YAP/TAZ in VSMCs led to Disheveled 3 (DVL3) nuclear translocation and upregulation of osteogenesis-associated genes independent of canonical Wnt/β-catenin signaling activation. Our data indicate that cytoplasmic YAP/TAZ interact with DVL3 to avoid its nuclear translocation and osteogenic differentiation, thereby maintaining the differentiated phenotype of VSMCs.
Indexed as
Identifiers
What Socratic 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 Socratic graph.