ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
CD8 T Cell-Derived Exosomal miR-186-5p Elicits Renal Inflammation via Activating Tubular TLR7/8 Signal Axis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- CD4 + T cell-derived exosomal miR-223-3p serves as a potential biomarker for systemic lupus erythematosus and attenuates lupus nephritis in NZBWF1/J mice.Journal of nanobiotechnology · 2026Article
- Generation of TCRγδ + T cells from human embryonic stem cells.Scientific reports · 2026Article
- miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review.Cells · 2026Review
- Identification and validation of biomarkers associated with lactic acid metabolism in diabetic nephropathy.PeerJ · 2026Article
- Identification and experimental validation of autophagy-related genes in focal segmental glomerulosclerosis by integrating bioinformatics and machine learning.Scientific reports · 2025Article
- Adriamycin-induced nephropathy models: elucidating CKD pathophysiology and advancing therapeutic strategies.Experimental animals · 2025Review
- Bioinformatics analysis and experimental validation of potential targets and pathways in chronic kidney disease associated with renal fibrosis.Journal of translational medicine · 2025Article
- Tubular epithelial cell-derived extracellular vesicles carrying serum amyloid A1 exacerbate sepsis-associated acute kidney injury by promoting NETs formation.Frontiers in immunology · 2025Article
- Lipin3 deficiency aggravates cisplatin induced acute kidney injury via activating Sirt1-p21-Caspase 3-GSDME pyroptosis pathway.International journal of biological sciences · 2025Article
- Emerging roles of exosomes in the diagnosis and treatment of kidney diseases.Frontiers in pharmacology · 2025Review
- miR-574-5p in epigenetic regulation and Toll-like receptor signaling.Cell communication and signaling : CCS · 2024Review
- Relationship of lncRNA FTX and miR-186-5p levels with diabetic peripheral neuropathy in type 2 diabetes and its bioinformatics analysis.Irish journal of medical science · 2024Article
- Potential biomarkers of recurrent FSGS: a review.BMC nephrology · 2024Review
- Longitudinal change of serum exosomal miR-186-5p estimates major adverse cardiac events in acute myocardial infarction patients receiving percutaneous coronary intervention.Frontiers in cardiovascular medicine · 2024Article
- CD8 T cells induce the peritubular capillary rarefaction during AKI to CKD transition.International journal of biological sciences · 2024Article
- Different origin-derived exosomes and their clinical advantages in cancer therapy.Frontiers in immunology · 2024Review
- CD8 T Cell-Derived Exosomal miR-186-5p Elicits Renal Inflammation via Activating Tubular TLR7/8 Signal Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Recent Advances in miRNA Biomarkers for Diagnosis and Prognosis of Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland)Review
- Post-Transplant Recurrence of Focal Segmental Glomerulosclerosis: Circulating Factors, Molecular Biomarkers, and Treatments.Kidney diseases (Basel, Switzerland)Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
T cells play an important role in the development of focal segmental glomerulosclerosis (FSGS). The mechanism underlying such T cell-based kidney disease, however, remains elusive. Here the authors report that activated CD8 T cells elicit renal inflammation and tissue injury via releasing miR-186-5p-enriched exosomes. Continuing the cohort study identifying the correlation of plasma level of miR-186-5p with proteinuria in FSGS patients, it is demonstrated that circulating miR-186-5p is mainly derived from activated CD8 T cell exosomes. Renal miR-186-5p, which is markedly increased in FSGS patients and mice with adriamycin-induced renal injury, is mainly delivered by CD8 T cell exosomes. Depleting miR-186-5p strongly attenuates adriamycin-induced mouse renal injury. Supporting the function of exosomal miR-186-5p as a key circulating pathogenic factor, intravenous injection of miR-186-5p or miR-186-5p-containing T cell exosomes results in mouse renal inflammation and tissue injury. Tracing the injected T cell exosomes shows their preferential distribution in mouse renal tubules, not glomerulus. Mechanistically, miR-186-5p directly activates renal tubular TLR7/8 signal and initiates tubular cell apoptosis. Mutating the TLR7-binding sequence on miR-186-5p or deleting mouse TLR7 largely abolishes renal tubular injuries induced by miR-186-5p or adriamycin. These findings reveal a causative role of exosomal miR-186-5p in T cell-mediated renal dysfunction.
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