ArticleJournal of molecular histology2022
Silence of MLK3 alleviates lipopolysaccharide-induced lung epithelial cell injury via inhibiting p53-mediated ferroptosis.
Article in Journal of molecular histology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- MLK3 promotes atherosclerosis by regulating ferroptosis in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- TARDBP Mediates the MAP3K11/SLC3A2/GPX4 Axis in Alzheimer's Disease Rats by Enhancing KRAS mRNA Stability.Journal of cellular and molecular medicine · 2026Article
- Role of Ferroptosis on Lung Epithelial Cells in Disease Progression and Treatment: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Role and mechanisms of autophagy, ferroptosis, and pyroptosis in sepsis-induced acute lung injury.Frontiers in pharmacology · 2024Review
- Review
- Multifaceted Roles of Ferroptosis in Lung Diseases.Frontiers in molecular biosciences · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute lung injury (ALI) is characterized with a high rate of morbidity and mortality. The injury and apoptosis of lung epithelial cells play crucial roles in the progression of ALI. Mixed lineage kinase 3 (MLK3) has been reported to be involved in the regulation of cellular biological functions, such as cell proliferation, apoptosis and ferroptosis. However, the effect of MLK3 exerted on ALI has not been reported. Here, LPS-stimulated MLE12 pulmonary epithelial cells were used as an in vitro model for ALI. In this research, LPS elevated the expression of MLK3 in MLE12 cells. The silence of MLK3 alleviated LPS-induced cell injury. Notably, LPS promoted ferroptosis through enhancing GSH depletion and the productions of MDA and iron, which was attenuated by MLK3 knockdown. Moreover, the silence of MLK3 inhibited p53 expression in LPS-induced cells along with a decrease in the expressions of p21 and Bax, while overexpressing p53 reversed these effects of MLK3 silence. Meanwhile, p53 overexpression reversed the positive effects of MLK3 knockdown on LPS-induced cell ferroptosis and injury. Together, our results confirmed that the silence of MLK3 alleviated LPS-induced lung epithelial cell injury by inhibiting p53-mediated ferroptosis.
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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 OpenQuestion graph.