ArticleCell death and differentiation2019
Transcription factor TEAD1 is essential for vascular development by promoting vascular smooth muscle differentiation.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- ZFP36 Protects against Abdominal Aortic Aneurysm Formation by Regulating Vascular Smooth Muscle Phenotypic Switch.Research (Washington, D.C.) · 2026Article
- Molecular architecture of mesoderm cells across early to middle stage of human embryo development at single-cell resolution.BMC molecular and cell biology · 2025Article
- MBNL loss of function in smooth muscle as a model for myotonic dystrophy associated gastrointestinal dysmotility.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- LncRNA MKLN1-AS promotes glioma tumorigenesis and growth via activating the Hippo pathway through miR-126-5p/TEAD1 axis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- NF2 is Essential for Human Endoderm Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Generation of a novel constitutive smooth muscle cell-specific Myh11-driven Cre mouse model.Journal of molecular and cellular cardiology · 2025Article
- Transcriptomics-driven exploration of genetic variation and peptide discovery in the sea anemones Anthopleura midori and Actinia equina.Scientific reports · 2025Article
- The Hippo effector TEAD1 regulates postnatal murine cerebellar development.Brain structure & function · 2025Article
- TEAD1-Mediated Trans-Differentiation of Vascular Smooth Muscle Cells into Fibroblast-Like Cells Contributes to the Stabilization and Repair of Disrupted Atherosclerotic Plaques.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cardiovascular Mettl3 Deficiency Causes Congenital Cardiac Defects and Postnatal Lethality in Mice.International journal of biological sciences · 2025Article
- TEAD1 Prevents Necroptosis and Inflammation in Cisplatin-Induced Acute Kidney Injury Through Maintaining Mitochondrial Function.International journal of biological sciences · 2025Article
- Targeting TEAD in cancer.Frontiers in oncology · 2025Review
- Hippo in smooth muscle - a therapeutic target in vascular diseases driven by aging and hypertension.Frontiers in physiology · 2025Review
- Neddylation drives myofibrillogenesis in the developing heart.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Suppression of smooth muscle cell inflammation by myocardin-related transcription factors involves inactivation of TANK-binding kinase 1.Scientific reports · 2024Article
- A novel mouse model carrying a gene trap insertion into the Hmgxb4 gene locus to examine Hmgxb4 expression in vivo.Physiological reports · 2024Article
- Article
- Wnt16 Promotes Vascular Smooth Muscle Contractile Phenotype and Function via Taz (Wwtr1) Activation in Male LDLR-/- Mice.Endocrinology · 2023Article
- Vascular smooth muscle-specific YAP/TAZ deletion triggers aneurysm development in mouse aorta.JCI insight · 2023Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
Abstract
TEAD1 (TEA domain transcription factor 1), a transcription factor known for the functional output of Hippo signaling, is important for tumorigenesis. However, the role of TEAD1 in the development of vascular smooth muscle cell (VSMC) is unknown. To investigate cell-specific role of Tead1, we generated cardiomyocyte (CMC) and VSMC-specific Tead1 knockout mice. We found CMC/VSMC-specific deletion of Tead1 led to embryonic lethality by E14.5 in mice due to hypoplastic cardiac and vascular walls, as a result of impaired CMC and VSMC proliferation. Whole transcriptome analysis revealed that deletion of Tead1 in CMCs/VSMCs downregulated expression of muscle contractile genes and key transcription factors including Pitx2c and myocardin. In vitro studies demonstrated that PITX2c and myocardin rescued TEAD1-dependent defects in VSMC differentiation. We further identified Pitx2c as a novel transcriptional target of TEAD1, and PITX2c exhibited functional synergy with myocardin by directly interacting with myocardin, leading to augment the differentiation of VSMC. In summary, our study reveals a critical role of Tead1 in cardiovascular development in mice, but also identifies a novel regulatory mechanism, whereby Tead1 functions upstream of the genetic regulatory hierarchy for establishing smooth muscle contractile phenotype.
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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.