ArticleExperimental & molecular medicine2021
TAZ as a novel regulator of oxidative damage in decidualization via Nrf2/ARE/Foxo1 pathway.
Article in Experimental & molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- FOXO transcription factors in Alzheimer's Disease: balancing neuroprotection and neuronal degeneration.Molecular biology reports · 2026Review
- Multifunctional Selenium-Sulfur-Doped Carbon Dots Nanozymes with Thioredoxin Reductase Activity for Regenerative Therapy of Infected Wounds.ACS applied materials & interfaces · 2026Article
- Mechanisms driving resistance to oxidative stress during endometrial stromal cell decidualization†.Biology of reproduction · 2026Review
- Regulated cell death in endometrial diseases: from molecular mechanisms to targeted therapies.Archives of toxicology · 2026Review
- PRMT3-mediated FOXO1 arginine methylation exacerbates oxidative stress-induced decidualization defects in the eutopic endometrium of endometriosis.Cellular and molecular life sciences : CMLS · 2025Article
- Proteasome stress activates YAP/TAZ through the RAP2-MAP4Ks-LATS1/2 pathway and its therapeutic implications in solid tumors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Regulation of Transcriptional Coactivator with PDZ-Binding Motif (TAZ) Expression by Estrogen in the Mouse Uterine Endometrium.Development & reproduction · 2025Article
- Mitochondrial dysfunction in pregnancy loss: a review.Molecular and cellular biochemistry · 2025Review
- Alterations in the Hippo Signaling Pathway During Adenogenesis Impairment in Postnatal Mouse Uterus.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- TAZ/NRF2 positive feedback loop contributes to proliferation in bladder cancer through antagonistic ferroptosis.Cell death discovery · 2025Article
- Precise targeting of transcriptional co-activators YAP/TAZ annihilates chemoresistant brCSCs by alteration of their mitochondrial homeostasis.Signal transduction and targeted therapy · 2025Article
- IBS008738, a TAZ activator, facilitates muscle repair and inhibits muscle injury in a mouse model of sport-induced injury.Cytotechnology · 2025Article
- TNFSF14The EMBO journal · 2024Article
- The Multiple Functions of HB-EGF in Female Reproduction and Related Cancer: Molecular Mechanisms and Targeting Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- 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 deficiency impairs the autophagy-lysosomal pathway through NRF2 dysregulation and lysosomal dysfunction.International journal of biological sciences · 2024Article
- Iron overload triggering ECM-mediated Hippo/YAP pathway in follicle development: a hypothetical model endowed with therapeutic implications.Frontiers in endocrinology · 2023Review
- Article
- HB-EGF induces mitochondrial dysfunction via estrogen hypersecretion in granulosa cells dependent on cAMP-PKA-JNK/ERK-CaInternational journal of biological sciences · 2022Article
- Research on the Mechanism of Asperosaponin VI for Treating Recurrent Spontaneous Abortion by Bioinformatics Analysis and Experimental Validation.Evidence-based complementary and alternative medicine : eCAM · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TAZ, as a crucial effector of Hippo pathway, is required for spermatogenesis and fertilization, but little is known regarding its physiological function in uterine decidualization. In this study, we showed that TAZ was localized in the decidua, where it promoted stromal cell proliferation followed by accelerated G1/S phase transition via Ccnd3 and Cdk4 and induced the expression or activity of stromal differentiation markers Prl8a2, Prl3c1 and ALP, indicating the importance of TAZ in decidualization. Knockdown of TAZ impeded HB-EGF induction of stromal cell proliferation and differentiation. Under oxidative stress, TAZ protected stromal differentiation against oxidative damage by reducing intracellular ROS and enhancing cellular antioxidant capacity dependent on the Nrf2/ARE/Foxo1 pathway. TAZ strengthened the transcriptional activity of Nrf2 which directly bound to the antioxidant response element (ARE) of Foxo1 promoter region. Additionally, silencing TAZ caused accumulation of intracellular ROS through heightening NOX activity whose blockade by APO reversed the disruption in stromal differentiation. Further analysis revealed that TAZ might restore mitochondrial function, as indicated by the increase in ATP level, mtDNA copy number and mitochondrial membrane potential with the reduction in mitochondrial superoxide. Additionally, TAZ modulated the activities of mitochondrial respiratory chain complexes I and III whose suppression by ROT and AA resulted in the inability of TAZ to defend against oxidative damage to stromal differentiation. Moreover, TAZ prevented stromal cell apoptosis by upregulating Bcl2 expression and inhibiting Casp3 activity and Bax expression. In summary, TAZ might mediate HB-EGF function in uterine decidualization through Ccnd3 and ameliorate oxidative damage to stromal cell differentiation via Nrf2/ARE/Foxo1 pathway.
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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.