ArticleEndocrinology, diabetes & metabolism2026
Diabetic Kidney Disease Progression Alleviated in Mice by ALKBH5-Mediated UC-MSCs-Derived Exosomes That Inhibit TRAF6 m6A Modification and Promote M2 Macrophage Polarisation.
Article in Endocrinology, diabetes & metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Functional Role of ALKBH5 in Kidney Injury: Insights Into Mechanisms and Therapeutic Potential.Journal of cellular biochemistry · 2026Review
- Diabetic Kidney Disease Progression Alleviated in Mice by ALKBH5-Mediated UC-MSCs-Derived Exosomes That Inhibit TRAF6 m6A Modification and Promote M2 Macrophage Polarisation.Endocrinology, diabetes & metabolism · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundDiabetic kidney disease (DKD) is a major diabetes complication with limited treatment options. Exosomes (Exo) from umbilical cord mesenchymal stem cells (UC-MSCs) have shown therapeutic promise. The role of alkylation repair homologue protein 5 (ALKBH5)-modified UC-MSCs Exo in regulating macrophage polarisation and alleviating DKD is investigated.
methodsDKD-associated inflammation was modelled by Lipopolysaccharide (LPS)/interferon-gamma (IFN-γ)-stimulated RAW264.7 macrophages. RT-qPCR and western blotting were employed to analyse mRNA and protein expression. Exosomes from ALKBH5-modified UC-MSCs were isolated and characterised. Macrophage polarisation (M1/M2) was assessed by flow cytometry, RT-qPCR, and enzyme-linked immunosorbent assay (ELISA). Tumor necrosis factor receptor-associated factor 6 (TRAF6) N6-methyladenosine (m6A) modification and expression were analysed via methylated RNA immunoprecipitation (MeRIP) and RNA immunoprecipitation (RIP) assays. The DKD model was established using spontaneous diabetic db/db mice. The renal function of mice was evaluated by ELISA and commercial assay kits. Hematoxylin-eosin (HE), periodic acid-Schiff (PAS), and Masson's trichrome staining were performed to assess the renal histopathology of mice.
resultsALKBH5 overexpression promoted M2 and inhibited M1 macrophage polarisation. ALKBH5 downregulated TRAF6 via m6A demethylation. ALKBH5-modified UC-MSCs Exo enhanced M2 polarisation and suppressed M1 phenotype in vitro. In DKD mice, ALKBH5-modified UC-MSCs Exo mitigated renal injury. Moreover, these exosomes enhanced anti-inflammatory responses and promoted M2 macrophage polarisation in DKD mice.
conclusionALKBH5-modified UC-MSCs Exo reduced TRAF6 expression by demethylating its m6A sites, promoting M2 macrophage polarisation and alleviating DKD progression. These findings suggested that ALKBH5-modified UC-MSCs Exo might represent a promising therapeutic approach for DKD.
Indexed as
Identifiers
What Socratic holds
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.