ArticleBiology direct2025
Nrf2/UBE3B protects against acute lung injury by inhibiting ferritinophagy through the ubiquitination of NCOA4.
Article in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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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Who cites it
3 citing papers in PubMed.
- The Iron Lung: Ferroptosis and Iron Regulation in Aging and Lung Diseases.Physiology (Bethesda, Md.) · 2026Review
- The E3 Ubiquitin Ligase UBE3B Regulates Synaptic Development and Cortical Network Activity.Autism research : official journal of the International Society for Autism Research · 2026Article
- NEDD4 suppresses ferroptosis in lung ischemia-reperfusion injury by ubiquitinating and degrading SLC1A5.Scientific reports · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundIron overload and ferroptosis are associated with intestinal ischemia and reperfusion (II/R)-induced acute lung injury (ALI). However, the mechanisms underlying the regulation of iron homeostasis remain unclear. Nrf2 regulates cellular iron homeostasis; nonetheless, its impact on ALI pathology and its underlying mechanism of action requires further investigation. Ubiquitin ligase E3B (UBE3B) plays a critical role in the proteasome pathway, which is essential for protein turnover and ubiquitin-mediated signaling. A recent study found that UBE3B plays a role in oxidative stress; nevertheless, it remains unknown whether its role is related to Nrf2. Furthermore, the exact role of UBE3B in ALI and its underlying mechanism remain largely uncharacterized. METHODS AND
resultsIn the present study, immunohistochemical analysis of UBE3B expression in type II alveolar epithelial cells (AECII) was conducted, and its expression was found to be decreased in II/R-ALI. Western blot analysis indicated that UBE3B hypoactivation may aggravate oxidative stress, thereby promoting ALI. Moreover, UBE3B was involved in iron metabolism dysfunction and ferroptosis. UBE3B deficiency enhanced the process of nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy and increased ferrous ion content, whereas overexpression of UBE3B reversed the harmful effects of Nrf2 knockdown on AECII, which may promote AECII ferroptosis.
conclusionsThis study highlights the role of the Nrf2/UBE3B/NCOA4 axis in AECII ferroptosis and II/R-ALI pathogenesis, suggesting that Nrf2 activation may be a promising strategy for ALI treatment.
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Registered trials
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 Socratic graph.