ArticleInflammation2024
Mesenchymal Stem Cells Regulate Microglial Polarization via Inhibition of the HMGB1/TLR4 Signaling Pathway in Diabetic Retinopathy.
Article in Inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 12 citations in OpenAlex.
- Stage-dependent signaling networks and therapeutic strategies in diabetic retinopathy: from neurovascular dysfunction to angiogenesis and fibrosis.Molecular biology reports · 2026Review
- Mesenchymal stem cell-mediated regulation of neuroinflammation and amyloid-β clearance: A promising therapeutic strategy for Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Review
- Innovative diabetes mellitus treatment strategies: Mesenchymal stem cell-based therapy and its impact on pro- and anti-inflammatory cytokines modulation.Journal of pharmaceutical analysis · 2026Review
- Extracellular Vesicles in Ophthalmology: From Natural Nanocarriers to Engineered Therapeutics.Bioengineering (Basel, Switzerland) · 2026Review
- Therapeutic potential of mesenchymal stem cells in ocular degenerative disorders.Journal of translational medicine · 2026Review
- Bone Marrow Mesenchymal Stem Cell-Derived Exosomal Let-7b-5p Reduces High Glucose-Induced Microglial Activation and Inflammation Through TLR4/ATF4.Mediators of inflammation · 2026Article
- Ferroptosis and the eye: bridging the gap between cell death and vision preservation.Frontiers in immunology · 2026Review
- Review: The role of microglia in diabetic retinopathy and its potential as a therapeutic target.Molecular vision · 2026Review
- Targeting the gut-retina axis: mechanistic insights and therapeutic prospects for diabetic retinopathy.Inflammopharmacology · 2025Review
- Sagittaria Sagittifolia Polysaccharide Ameliorates Diabetic Retinopathy in Mice via Inhibiting TLR4-Mediated Microglial Activation.Molecular neurobiology · 2025Article
- Macrophage polarization in diabetic vascular complications: mechanistic insights and therapeutic targets.Journal of translational medicine · 2025Review
- Mesenchymal stem cells and mesenchymal stem cell-derived exosomes: a promising strategy for treating retinal degenerative diseases.Molecular medicine (Cambridge, Mass.) · 2025Review
- Non-Linear Relationship Between Fasting C-Peptide and Retinopathy in Patients with Type 2 Diabetes Mellitus - A Retrospective Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic retinopathy (DR) is recognized as the most prevalent retinal degenerative disorder. Inflammatory response usually precedes microvascular alteration and is the primary factor of diabetic retinopathy. Activated microglia express many pro-inflammatory cytokines that exacerbate retina inflammation and disruption. In the present study, we found that MSCs alleviated blood-retina barrier (BRB) breakdown in diabetic rats, as evidenced by reduced retinal edema, decreased vascular leakage, and increased occludin expression. The MSC-treated retinal microglia exhibited reduced expression of M1-phenotype markers in the diabetic rats, including inducible nitric oxide synthase (iNOS), CD16, and pro-inflammatory cytokines. On the other hand, MSCs increased the expression of M2-phenotype markers, such as arginase-1 (Arg-1), CD206, and anti-inflammatory cytokines. HMGB1/TLR4 signaling pathway is activated in DR and inhibited after MSC treatment. Consistent with in vivo evidence, MSCs drove BV2 microglia toward M2 phenotype in vitro. Overexpression of HMGB1 in microglia reversed the effects of MSC treatment, suggesting HMGB1/TLR4 pathway is necessary for MSCs' regulatory effects on microglia polarization. Collectively, MSCs exert beneficial effects on DR by polarizing microglia from M1 toward M2 phenotype via inhibiting the HMGB1/TLR4 signaling pathway.
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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.