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May 16, 2026Ecotoxicology and Environmental Safety0 citationsOpen Access

Chrysin reshapes ferroptosis sensitivity to reverse nickel refining fumes-induced lung injury via the miR-210/ANGPTL4 signaling axis mediated by the PHD1/HIF-1α pathway

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WYWenxue YaoRWRuize WuQSQianqian Sun

Key Points

  • This study aims to explore the role of the PHD1/HIF-1α/miR-210/ANGPTL4 pathway in nickel-induced ferroptosis suppression and lung injury.
  • Examined the impact of chrysin on nickel-induced lung injury in Beas-2B cells.
  • Evaluated the signaling pathways involved, specifically PHD1/HIF-1α and miR-210/ANGPTL4.
  • Utilized cellular models to assess ferroptosis sensitivity and malignant transformation.
  • Chrysin significantly reversed nickel-induced suppression of ferroptosis in 2B-Ni cells.
  • The PHD1/HIF-1α/miR-210/ANGPTL4 pathway was confirmed as a mediator of this effect.
  • Findings support the potential for chrysin in treating nickel carcinogenesis and lung injury.

Abstract

can reverse this effect. In summary, this study confirms that the PHD1/HIF-1α/miR-210/ANGPTL4 pathway mediates Ni-induced suppression of ferroptosis, thereby promoting malignant transformation in Beas-2B cells. Conversely, chrysin mitigates Ni-induced lung injury by regulating PHD1/HIF-1α-induced ferroptosis in 2B-Ni cells. These findings offer essential theoretical support and potential targets for evaluating Ni's carcinogenic risk and developing ferroptosis-targeted anti-tumor therapies.

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Cite This Study

Yao et al. (2026) studied this question.

synapsesocial.com/papers/6a0808ffa487c87a6a40b113https://doi.org/10.1016/j.ecoenv.2026.120239
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