ArticleScientific reports2025
Nrf2 alleviates excessive deposition of extracellular matrix in mammary fibrosis through TGF/Smad and ROS signals.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- ZhuJing Pill retards lens-induced myopia progression by improving ciliary muscle mitochondrial function via KEAP1/NRF2-TGF-β axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Hexavalent Chromium Exposure Disrupts Cardiac Development in Chicken Embryos Through Oxidative Stress and Activation of TGFβ1/COL3A1 Pathway in Chick Embryos.Cardiovascular toxicology · 2026Article
- Palmatine Attenuates LPS-Induced EMT in MAC-T Cells and Mammary Fibrosis in Mice, with Suppression of NF-κB/TGF-β1/Smad Signaling In Vivo.Animals : an open access journal from MDPI · 2026Article
- Therapeutic potential of ginseng and its bioactive compounds in inflammatory bowel disease: current evidence and future directions.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Mammary fibrosis poses a significant health threat to lactating mothers, as it alters milk composition and adversely affects infant health. Nuclear factor erythroid 2-related factor 2 (Nrf2) serves as a master regulator of the cellular adaptive antioxidant response and plays a pivotal role in various biological processes, including anti-inflammatory effects, antioxidant responses, and metabolic regulation. However, the role and mechanism of Nrf2 in mammary fibrosis remain unreported. This study employed a mouse model to investigate the impact of Nrf2 on TGF-β1-induced mammary fibrosis and its underlying mechanisms. Both in vitro and in vivo experiments demonstrated that knockout or inhibition of Nrf2 significantly exacerbated fibrosis-related phenotypic markers. Conversely, Nrf2 activation suppressed the upregulation of fibrotic proteins and mRNAs, such as Vim, α-SMA, and Collagen 1, thereby alleviating mammary fibrosis in mice. Further mechanistic studies revealed that Nrf2 modulates mitochondrial autophagy and mitigates mitochondrial damage to regulate ROS generation, subsequently influencing mammary fibrosis via the TGF/Smad signaling pathway. In conclusion, this study reveals a novel function of Nrf2 in mitigating mammary fibrosis, suggesting potential therapeutic strategies for its treatment and prevention.
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