ArticleNature metabolism2022
A YAP/TAZ-TEAD signalling module links endothelial nutrient acquisition to angiogenic growth.
Article in Nature metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
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Who cites it
70 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Systematic Review of Interleukin-35 in Endothelial Dysfunction: A New Target for Therapeutic Intervention.Mediators of inflammation · 2025Pooled it
- Endothelial Epac1 facilitates YAP/TAZ controlled melanoma growth and angiogenesis.Angiogenesis · 2026Article
- Interactions between circular RNAs (circRNAs) and the Hippo pathway in cancer.Molecular biology reports · 2026Review
- LATS1/2 inactivation drives a distinct venous endothelial cell response that contributes to fibrotic remodeling of the lung.Science advances · 2026Article
- Macrophage programming in systemic sclerosis: Niches, networks, and translational horizons.Seminars in immunopathology · 2026Review
- Integrating short-read and long-read single-cell transcriptomics of pig pituitary reveals mechanisms of high-altitude hypoxia adaptation.PLoS genetics · 2026Article
- Article
- Flow-Induced Yap/Taz Signaling Balances Endothelial and Hematopoietic Stem Cell Fates.bioRxiv : the preprint server for biology · 2026Article
- MYCT1-IFITM2/3 interaction links endothelial endolysosomal trafficking to white adipose tissue expansion.The Journal of experimental medicine · 2026Article
- TEAD1 Enhances Exosome Secretion and Promotes Exosome-Mediated Tissue Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- Review
- Celecoxib Inhibits Vasculogenic Mimicry and Induces Apoptosis in the D17 Canine Osteosarcoma Cell Line via the COX-2/PGE2 Signaling Axis.Veterinary sciences · 2026Article
- Loss of Endothelial YAP/TAZ Reduces the Size of Chronic Stroke Lesions and Alters the Endothelial Environment.Journal of the American Heart Association · 2026Article
- Endothelial Yes-Associated Protein/Transcription Regulator 1: From Angiogenic Driver to Poststroke Immune Gatekeeper.Journal of the American Heart Association · 2026Article
- Defining the vascular niche of human adipose tissue across metabolic states.Nature metabolism · 2026Article
- Targeting the 5-HTActa pharmacologica Sinica · 2026Article
- YAP1 Is a Crucial Nexus in the Tumor Microenvironment.Current medical science · 2026Review
- Temporal vascular pattern remodeling mediated by the FHL2/sFRP2 signaling pathway in tenocytes affects tendon repair and regeneration.Experimental & molecular medicine · 2025Article
- Endothelial Arginine Metabolism in Angiogenesis: Mechanistic Insights from Tissue Repair to Tumor Progression.Metabolites · 2025Review
10 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 10 institutions in 7 countries.
Funding
Abstract
Angiogenesis, the process by which endothelial cells (ECs) form new blood vessels from existing ones, is intimately linked to the tissue's metabolic milieu and often occurs at nutrient-deficient sites. However, ECs rely on sufficient metabolic resources to support growth and proliferation. How endothelial nutrient acquisition and usage are regulated is unknown. Here we show that these processes are instructed by Yes-associated protein 1 (YAP)/WW domain-containing transcription regulator 1 (WWTR1/TAZ)-transcriptional enhanced associate domain (TEAD): a transcriptional module whose function is highly responsive to changes in the tissue environment. ECs lacking YAP/TAZ or their transcriptional partners, TEAD1, 2 and 4 fail to divide, resulting in stunted vascular growth in mice. Conversely, activation of TAZ, the more abundant paralogue in ECs, boosts proliferation, leading to vascular hyperplasia. We find that YAP/TAZ promote angiogenesis by fuelling nutrient-dependent mTORC1 signalling. By orchestrating the transcription of a repertoire of cell-surface transporters, including the large neutral amino acid transporter SLC7A5, YAP/TAZ-TEAD stimulate the import of amino acids and other essential nutrients, thereby enabling mTORC1 activation. Dissociating mTORC1 from these nutrient inputs-elicited by the loss of Rag GTPases-inhibits mTORC1 activity and prevents YAP/TAZ-dependent vascular growth. Together, these findings define a pivotal role for YAP/TAZ-TEAD in controlling endothelial mTORC1 and illustrate the essentiality of coordinated nutrient fluxes in the vasculature.
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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.