ArticleInflammation2025
Dimethyloxallyl Glycine Preconditioning Promotes the Anti-inflammatory and Anti-fibrotic Effects of Human Umbilical Cord Mesenchymal Stem Cells on Kidney Damage in Systemic Lupus Erythematosus Related to TGF-β/Smad Signaling Pathway.
Article in Inflammation, 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 trial behind it
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Who cites it
6 citing papers in PubMed.
- DMOG Enhances hUC-MSCs Paracrine Activity to Promote Endometrial Epithelial Cells Reconstitution Via VSELs Formation in Ovariectomized Mice.Stem cell reviews and reports · 2026Article
- Pretreated mesenchymal stromal cells and their secretome for kidney disease: mechanisms and applications.Stem cell research & therapy · 2026Review
- Stem cell-derived extracellular vesicles as immunomodulatory agents: targeting pathological crosstalk in systemic lupus erythematosus and multiple sclerosis.Frontiers in medicine · 2026Review
- Urine-Derived CD105-Positive Exosome Promotes Macrophage M1 Polarization Through the TGF-β1/Smad3 Signaling Axis To Exacerbate Lupus Nephritis.Inflammation · 2025Article
- Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025Review
- Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease lacking effective treatments without adverse effects. Dimethyloxallyl glycine (DMOG) enhanced mesenchymal stem cells (MSC) capabilities, but it remains unclear how DMOG-pretreatment of MSCs augments their SLE treatment. Here, we explore the therapeutic potential of DMOG-pretreated human umbilical cord MSCs (hUC-MSCs) in a mouse lupus nephritis (LN) model. In vitro experiments showed that DMOG could alleviate the mRNA levels of tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-6 and increase the mRNA level of IL-13 in lipopolysaccharide (LPS)-induced inflammation in hUC-MSCs. DMOG enhanced the migratory and invasive abilities of the hUC-MSCs. In vivo animal studies revealed that DMOG-pretreated hUC-MSCs exhibited more pronounced inhibition of lymphadenectasis and reduced kidney weight and urinary protein content than MSCs alone. DMOG-pretreated hUC-MSCs improved renal morphological structure and alleviated inflammatory cell infiltration and renal fibrosis, evidenced by the reduced mRNA levels of fibrosis markers, including fibronectin (Fn), collagen alpha-1 chain (Colα1), collagen alpha-3 chain (Colα3), and TNF-α, IFN-γ, and IL-6 cytokines. Further investigation revealed that DMOG-pretreated hUC-MSCs down-regulated the expressions of transforming growth factor (Tgf)-β1 and its downstream effectors Smad2 and Smad3, recognized as central mediators in renal fibrosis (P < 0.05). The findings suggest that DMOG-pretreated hUC-MSCs can augment the therapeutic efficacy of hUC-MSCs in LN by enhancing their anti-inflammatory and antifibrotic effects, and the TGF-β/Smad signaling pathway may be involved in this process.
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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.