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<p>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.</p>

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Nrf2 alleviates excessive deposition of extracellular matrix in mammary fibrosis through TGF/Smad and ROS signals

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月10日

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  • Xingchi Kan,
  • Ping Xu,
  • Minghang Yu,
  • Wenjin Guo,
  • Yu Cao,
  • Guiqiu Hu,
  • Juxiong Liu,
  • Shoupeng Fu,
  • Junlong Bi

摘要

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.