ArticleJournal of immunology research2024
Taz/Tead1 Promotes Alternative Macrophage Activation and Kidney Fibrosis via Transcriptional Upregulation of Smad3.
Article in Journal of immunology research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The hippo-YAP1/TEAD1-SLC7A5 axis: uncovering a novel therapeutic target for oxalate-induced renal tubular ferroptosis.Redox report : communications in free radical research · 2026Article
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- γδ T cell-stromal networks modulate matrix composition and vascularity in foreign body response.Nature communications · 2026Article
- Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney.Life (Basel, Switzerland) · 2025Review
- In vitro models to mimic tumor endothelial cell-mediated immune cell reprogramming in lung adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Multi-Omics Alterations in Rat Kidneys upon Chronic Glyphosate Exposure.Biomolecules · 2025Article
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Authors and funding
8 authors.
Funding
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Abstract
Macrophage alternative activation is involved in kidney fibrosis. Previous researches have documented that the transcriptional regulators Yes-associated protein (Yap)/transcriptional coactivator with PDZ-binding motif (Taz) are linked to organ fibrosis. However, limited knowledge exists regarding the function and mechanisms of their downstream molecules in regulating macrophage activation and kidney fibrosis. In this paper, we observed that the Hippo pathway was suppressed in macrophages derived from fibrotic kidneys in mice. Knockout of Taz or Tead1 in macrophages inhibited the alternative activation of macrophages and reduced kidney fibrosis. Additionally, by using bone marrow-derived macrophages (BMDMs), we investigated that knockout of Taz or Tead1 in macrophages impeded both cell proliferation and migration. Moreover, deletion of Tead1 reduces p-Smad3 and Smad3 abundance in macrophages. And chromatin immunoprecipitation (ChIP) assays showed that Tead1 could directly bind to the promoter region of Smad3. Collectively, these results indicate that Tead1 knockout in macrophages could reduce TGF
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