ArticleNaunyn-Schmiedeberg's archives of pharmacology2024
Inhibition of ALKBH5 inhibits inflammation and excessive proliferation by promoting TRIM13 m6A modifications in glomerular mesangial cells.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Functional Role of ALKBH5 in Kidney Injury: Insights Into Mechanisms and Therapeutic Potential.Journal of cellular biochemistry · 2026Review
- Tripartite motif 13 orchestrates endoplasmic reticulum-associated degradation and endoplasmic reticulum-phagy to modulate dendritic cell-mediated immune responses in sepsis.Burns & trauma · 2026Article
- 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
- RBM15-dependent m6A modification mediates progression of non-small cell lung cancer cells.Molecular medicine (Cambridge, Mass.) · 2024Article
- The role of RNA m6A demethylase ALKBH5 in the mechanisms of fibrosis.Frontiers in cell and developmental biology · 2024Review
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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
Chronic glomerulonephritis (CGN) refers to the inflammation of glomeruli in the kidneys. Glomerular mesangial cells (GMCs) play a pivotal role in the development of CGN. In the present study, we investigated the impact of ALKBH5, a m6A demethylase, on inflammation and hyperproliferation in mouse glomerular mesangial cells (MMCs) and elucidated the molecular mechanisms contributing to CGN. Western blotting and reverse transcriptase-polymerase chain reaction (RT-qPCR) were employed to evaluate the expression of ALKBH5 and TRIM13. In addition, enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory factors (IL-1β, TNF-α, and IL-10) in the lipopolysaccharide (LPS)-induced MMCs supernatant. Methylated RNA immunoprecipitation (MeRIP) was performed to investigate the effect of ALKBH5 on the levels of TRIM13-m6A mRNA. The stability of TRIM13 mRNA was evaluated using an actinomycin D assay. Significantly elevated expression of ALKBH5 was found in LPS-induced MMCs. Interference with ALKBH5 expression inhibited inflammation and excessive proliferation in LPS-induced MMCs. Moreover, interfering with ALKBH5 expression significantly reduced the levels of TRIM13-m6A modification. The overexpression of TRIM13 in MMCs reversed the inflammation and proliferation induced by ALKBH5 interference. In addition, interference with TRIM13 expression inhibited the activation of the NF-κB pathway and suppressed inflammation and proliferation in MMCs. Inhibiting ALKBH5 hinders inflammation and hyperproliferation by improving TRIM13-m6A modification in glomerular MCs. We believe these findings will further provide insights into the molecular mechanisms and potential therapeutic targets for CGN.
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