ArticleNature communications2022
The TFEB-TGIF1 axis regulates EMT in mouse epicardial cells.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- PARP1 stabilizes FOXN3 to suppress pulmonary fibrosis through p38-related feedback regulation.Science advances · 2026Article
- Advances in Epicardial Biology: Insights from Development, Regeneration, and Human Cardiac Organoids.Journal of cardiovascular development and disease · 2025Review
- The Role ofChronic obstructive pulmonary diseases (Miami, Fla.) · 2025Article
- Bioceramics-enhanced patch activates epicardial epithelial-to-mesenchymal transition via Notch pathway for cardiac repair.Science advances · 2025Article
- Phosphorylation of FOXN3 by NEK6 promotes pulmonary fibrosis through Smad signaling.Nature communications · 2025Article
- Epicardium-myocardium crosstalk orchestrates heart development.Frontiers in cell and developmental biology · 2025Review
- TFEB controls syncytiotrophoblast formation and hormone production in placenta.Cell death and differentiation · 2024Article
- LncRNAs in theInternational journal of molecular sciences · 2024Article
- Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024Review
- Key mRNAs and lncRNAs of pituitary that affect the reproduction of FecB + + small tail han sheep.BMC genomics · 2024Article
- A Novel Bioswitchable miRNA Mimic Delivery System: Therapeutic Strategies Upgraded from Tetrahedral Framework Nucleic Acid System for Fibrotic Disease Treatment and Pyroptosis Pathway Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Novel Insights into the Molecular Mechanisms Governing Embryonic Epicardium Formation.Journal of cardiovascular development and disease · 2023Review
- TFEB inhibition induces melanoma shut-down by blocking the cell cycle and rewiring metabolism.Cell death & disease · 2023Article
- E15.5 Mouse Embryo Micro-CT Using a Bruker Skyscan 1172 Micro-CT.Bio-protocol · 2023Article
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a complex and pivotal process involved in organogenesis and is related to several pathological processes, including cancer and fibrosis. During heart development, EMT mediates the conversion of epicardial cells into vascular smooth muscle cells and cardiac interstitial fibroblasts. Here, we show that the oncogenic transcription factor EB (TFEB) is a key regulator of EMT in epicardial cells and that its genetic overexpression in mouse epicardium is lethal due to heart defects linked to impaired EMT. TFEB specifically orchestrates the EMT-promoting function of transforming growth factor (TGF) β, and this effect results from activated transcription of thymine-guanine-interacting factor (TGIF)1, a TGFβ/Smad pathway repressor. The Tgif1 promoter is activated by TFEB, and in vitro and in vivo findings demonstrate its increased expression when Tfeb is overexpressed. Furthermore, Tfeb overexpression in vitro prevents TGFβ-induced EMT, and this effect is abolished by Tgif1 silencing. Tfeb loss of function, similar to that of Tgif1, sensitizes cells to TGFβ, inducing an EMT response to low doses of TGFβ. Together, our findings reveal an unexpected function of TFEB in regulating EMT, which might provide insights into injured heart repair and control of cancer progression.
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