ArticleRespiratory research2024
Ferritinophagy mediated by the AMPK/ULK1 pathway is involved in ferroptosis subsequent to ventilator-induced lung injury.
Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Mechanical ventilation activates PERK/eIF2α and NOD1 pathways that contribute to NF-κB-driven inflammation in VILI.Respiratory research · 2026Article
- Autophagy-epithelial-mesenchymal transition crosstalk in acute respiratory distress syndrome: Mechanistic insights and therapeutic perspectives (Review).Experimental and therapeutic medicine · 2026Review
- Ventilator-Induced Lung Injury: Mechanotransduction and Potential Therapeutic Targets.MedComm · 2026Review
- Ferroptosis-dependent small extracellular vesicles ULK1 enhances mitophagy and suppresses breast cancer migration.Hereditas · 2026Article
- NCOA4 as a regulatory switch linking DNA damage to lipid peroxidation in radiation response.Frontiers in cell and developmental biology · 2026Review
- Revisiting ventilator-induced lung injury: from mechanical power to immunometabolic interaction.Frontiers in immunology · 2026Review
- Ferroptosis in Diabetic Cardiomyopathy and Atherosclerosis: Mechanisms and Clinical Prospects.International journal of molecular sciences · 2025Review
- Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Mechanical ventilation (MV) remains a cornerstone of critical care; however, its prolonged application can exacerbate lung injury, leading to ventilator-induced lung injury (VILI). Although previous studies have implicated ferroptosis in the pathogenesis of VILI, the underlying mechanisms remain unclear. This study investigated the roles of ferritinophagy in ferroptosis subsequent to VILI. Using C57BL/6J mice and MLE-12 cells, we established both in vivo and in vitro models of VILI and cyclic stretching (CS)-induced cellular injury. We assessed lung injury and the biomarkers of ferroptosis and ferritinophagy, after appropriate pretreatments. This study demonstrated that high tidal volumes (HTV) for 4 h enhanced the sensitivity to ferroptosis in both models, evidenced by increased intracellular iron levels, lipid peroxidation and cell death, which can be mitigated by ferrostatin-1 treatment. Notably, nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy contributed to ferroptosis in VILI. Inhibition of autophagy with 3-methyladenine or NCOA4 knockdown decreased intracellular Fe
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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.