ArticleCell proliferation2025
Inhibition of Alkbh5 Attenuates Lipopolysaccharide-Induced Lung Injury by Promoting Ccl1 m6A and Treg Recruitment.
Article in Cell proliferation, 2025. 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.
The trial behind it
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.
- ALKBH5-Driven m6A Demethylation Boosts Inflammation and Autophagy in LPS-Stimulated Macrophages.Immunity, inflammation and disease · 2026Article
- N6-methyladenosine methylation in acute lung injury: Mechanisms and research progress.Journal of intensive medicine · 2026Review
- The Mechanism of Oxidative Stress in Pulmonary Fibrosis and Research Progress.Antioxidants (Basel, Switzerland) · 2026Review
- Retinal ALKBH5 inhibition induces myopia protection through selective regulation of ERK1/2 signaling.Journal of translational medicine · 2025Article
- Inhibition of Alkbh5 Attenuates Lipopolysaccharide-Induced Lung Injury by Promoting Ccl1 m6A and Treg Recruitment.Cell proliferation · 2025Article
- Decoding the immunoregulatory functions of ALKBH5 in the tumor microenvironment.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
This paper discussed the role of AlkB homologue 5 (Alkbh5) in the progression of lipopolysaccharide (LPS)-induced acute lung injury (ALI). LPS-induced ALI models were established in Alkbh5 knockout (KO) and knock-in (KI) mice. The m6A levels in lung tissues were analysed using m6A dot assays. The lung injury was analysed by determining ALI-related markers and histological staining. Mouse MLE12 cells were exposed to LPS for in vitro experiments, and the influence of Alkbh5 on cell viability, apoptosis and reactive oxygen species (ROS) production was analysed. RNA-seq analysis was performed to analyse gene changes upon Alkbh5 deficiency. Functions of the Alkbh5-C-C motif chemokine ligand 1 (Ccl1) cascade in ALI were further verified using the Alkbh5 antagonist DDO-2728 and a recombinant protein of Ccl1 (mCcl1). Alkbh5 was upregulated in lung tissues following LPS exposure. Alkbh5 knockout in mice mitigated LPS-induced lung injury, as indicated by reduced serum levels of lung injury markers and reduced immune cell infiltration, fibrosis and apoptosis. Conversely, Alkbh5 overexpression in mice resulted in reverse trends. In vitro, Alkbh5 knockdown in MLE12 cells enhanced cell viability while reducing cell apoptosis and ROS production. Mechanistically, Alkbh5 was found to bind to and destabilise Ccl1 mRNA, leading to increased Treg recruitment. Treatment with DDO-2728 or mCcl1 in mice increased Treg infiltration, thus improving lung tissue pathology and reducing lung injury. This study suggests that Alkbh5 is implicated in ALI progression by reducing Ccl1-mediated Treg recruitment, making it a promising target for ALI management.
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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.