ArticleTurkish journal of biology = Turk biyoloji dergisi2025
Apigenin attenuates ischemia-reperfusion-induced pulmonary ferroptosis and fibrosis by activating the Nrf2/HO-1/GPX4 axis in mice.
Article in Turkish journal of biology = Turk biyoloji dergisi, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Evolution in lung IRI cell death research: a 20-year global bibliometric study (2005-2024).Annals of medicine and surgery (2012) · 2026Review
- NRF2 as a Therapeutic Target in Dermatological Disorders: Mechanisms and Molecules.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Nrf2 alleviates excessive deposition of extracellular matrix in mammary fibrosis through TGF/Smad and ROS signals.Scientific reports · 2025Article
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Authors and funding
5 authors.
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Abstract
Background/aim: Acute lung injury (ALI) is a major cause of morbidity and mortality after lung ischemia-reperfusion injury (LIRI). In recent years, pulmonary ferroptosis and its associated fibrosis have been recognized as important causes of LIRI. The purpose of this study is to investigate apigenin (APG) as a potential therapeutic target for treating LIRI-induced pulmonary ferroptosis and fibrosis. Materials and methods: A rat model of LIRI was established and the rats were randomly divided into three groups, a sham group, a LIRI group, and an APG group. The pathological changes of the lung tissue were evaluated using hematoxylin-eosin staining and Masson's trichrome staining. Alterations in lung function were assessed using the pulmonary permeability index, myeloperoxidase, and wet-to-dry weight ratio. The pulmonary ferroptosis levels were evaluated by testing Fe Results: The results show that APG pretreatment relieves LIRI-induced pulmonary pathological damage and functional abnormalities in rats. In addition, APG administration can significantly improve LIRI-induced pulmonary ferroptosis and fibrosis levels. However, using Nrf2 inhibitors to block the Nrf2/HO-1/GPX4 pathway significantly reversed these therapeutic effects. Conclusion: These findings suggest that APG protects against LIRI-induced ferroptosis and fibrosis of lung tissues via the activation of the Nrf2/HO-1/GPX4 axis.
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