ArticleMolecular therapy. Nucleic acids2022
TAZ ameliorates the microglia-mediated inflammatory response via the Nrf2-ROS-NF-κB pathway.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 63 citations in OpenAlex.
- Metabolomics and Mechanistic Approaches Reveal the Synergistic and Attenuating of Rubus chingii Hu on Tripterygium Glycoside Tablets in the Treatment of Rheumatoid Arthritis.Chemistry & biodiversity · 2026Article
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- Hippo-YAP/TAZ Signaling in Astrocytes and Microglia: Role in Neuroinflammation, Neurodegeneration and Glial Tumors.International journal of molecular sciences · 2026Review
- Huangqi Baihe Granules alleviate chemotherapy-induced intestinal mucositis in Drosophila and mice.AMB Express · 2026Article
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- In Situ Proliferating Peptide Nanoparticle Augments Multi-Target Intervention of Secondary Brain Damage Following Subarachnoid Hemorrhage.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cuproptosis and cuproptosis-related cell death and genes: mechanistic links to spermatogenic cell death.Cell death discovery · 2025Review
- Therapeutic potential of 3-acetyl coumarin against polycystic ovarian syndrome induced by letrozole using female rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Hippo-YAP/TAZ-ROS signaling axis regulates metaflammation induced by SelenoM deficiency in high-fat diet-derived obesity.Journal of advanced research · 2025Article
- The multifaceted roles of the transcriptional coactivator TAZ in extravillous trophoblast development of the human placenta.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- IBS008738, a TAZ activator, facilitates muscle repair and inhibits muscle injury in a mouse model of sport-induced injury.Cytotechnology · 2025Article
- The active roles ofFrontiers in veterinary science · 2025Article
- Role of NRF2 in Pathogenesis of Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2024Review
- DDO1002, an NRF2-KEAP1 inhibitor, improves hematopoietic stem cell aging and stress response.Life medicine · 2024Article
- Curcumin loaded hydrogel with double ROS-scavenging effect regulates microglia polarization to promote poststroke rehabilitation.Materials today. Bio · 2024Article
- β-1,4-Galactosyltransferase 1 protects against cerebral ischemia injury in mice by suppressing ferroptosis via the TAZ/Nrf2/HO-1 signaling pathway.CNS neuroscience & therapeutics · 2024Article
- TAZ reverses the inhibitory effects of LPS on the osteogenic differentiation of human periodontal ligament stem cells through the NF-κB signaling pathway.BMC oral health · 2024Article
- An Exploration of the Antioxidative and Anti-Inflammatory Role ofFoods (Basel, Switzerland) · 2024Article
- A mixture of extracts from natural ingredients reduces the neurotoxic polarization of microglia via modulating NF-κB/NF-E2-related factor 2 activation.Food science & nutrition · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional co-activator with PDZ-binding motif (TAZ), one of core modules of the Hippo pathway, involves inflammatory cell infiltration in the liver, but little information is available regarding its physiological function in the microglia-mediated inflammatory response. Here we revealed that activation of TAZ prevented microglia production of proinflammatory cytokines, indicating TAZ's importance in anti-inflammation. After translocation into the nucleus, TAZ interacted with transcriptional enhanced associate domain (TEAD) and bound to the promoter of nuclear factor erythroid 2-related factor 2 (Nrf2), whose blockage caused inability of TAZ to improve inflammation, implying that Nrf2 is a direct target of TAZ. Further analysis showed that TAZ induced Nrf2 nuclear translocation to enhance antioxidant capacity with attenuation of oxidative stress and the inflammatory response. Under inflammatory conditions, TAZ impeded mitochondrial dysfunction, as indicated by amelioration of ATP levels, mtDNA copy numbers, and mitochondrial membrane potential with an obvious reduction in mitochondrial superoxide, but this impediment was neutralized by blockage of Nrf2. TAZ hindered opening of the mitochondrial permeability transition pore, restrained release of cytochrome
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