ArticleCell communication and signaling : CCS2023
Proximal tubule-derived exosomes contribute to mesangial cell injury in diabetic nephropathy via miR-92a-1-5p transfer.
Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- The lactate-lactylation axis in renal fibrosis: potential mechanisms in diabetic kidney disease.Annals of medicine · 2025Pooled it
- The dual role of exosomes in renal fibrosis and their potential for clinical translational applications.Renal failure · 2026Review
- Extracellular Vesicle-Derived MicroRNAs as Early Diagnostic Biomarkers of Diabetic Nephropathy and Cardiovascular Diseases in Type 2 Diabetes.International journal of molecular sciences · 2026Review
- Glomerulo-Tubular Crosstalk in Diabetic Kidney Disease: From Pathophysiology to Novel Therapeutics.Electrolyte & blood pressure : E & BP · 2026Review
- Leveraging extracellular vesicle biology for novel tests and therapeutics for kidney fibrosis.Clinical and translational medicine · 2026Review
- Shedding light on the role of extracellular vesicles in renal fibrosis.Fundamental research · 2026Review
- Exosomal MicroRNAs as theranostic tools in type 2 diabetes and its complications: mechanistic insights and clinical implications.Diabetology & metabolic syndrome · 2026Review
- From pathogenic carriers to therapeutic hope: the dual role and translational prospects of exosomes in diabetic kidney disease.Frontiers in endocrinology · 2026Review
- The role of extracellular vesicles in kidney disease progression.Kidney research and clinical practice · 2026Article
- Exosome-mediated cell-cell communication: a new perspective on the mechanisms and therapeutic potential of diabetic microvascular complications.Frontiers in pharmacology · 2026Review
- Smurf2 knockdown attenuates the progression of diabetic nephropathy by inhibiting mesangial cell proliferation and fibrosis through suppressing EYA2 ubiquitination.Renal failure · 2025Article
- NF-κB p65 mediated lnc-Traf3ip2 exacerbates renal fibrosis in diabetic kidney disease.Acta diabetologica · 2025Article
- Exosomes applications in kidney diseases.Molecular biology reports · 2025Review
- Integrating bioinformatics and machine learning to identify glomerular injury genes and predict drug targets in diabetic nephropathy.Scientific reports · 2025Article
- Role of exosomes in pathogenesis, diagnosis, and treatment of diabetic nephropathy.BMC nephrology · 2025Review
- Article
- Extracellular vesicles derived from mesenchymal stem cells alleviate renal fibrosis via the miR-99b-5p/mTOR/autophagy axis in diabetic kidney disease.Stem cell research & therapy · 2025Article
- Research progress on non-coding RNA regulatory networks and targeted therapy in diabetic nephropathy.Frontiers in endocrinology · 2025Review
- Mesangial Cells in Diabetic Kidney Disease: From Mechanisms to Therapeutic Implications.International journal of biological sciences · 2025Review
- Urinary exosomes as promising biomarkers for early kidney disease detection.American journal of clinical and experimental urology · 2025Review
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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
backgroundDiabetic nephropathy (DN) is an increasing threat to human health and regarded to be the leading cause of end-stage renal disease worldwide. Exosomes delivery may play a key role in cross-talk among kidney cells and the progression of DN. However, the mechanisms underlying exosomes in DN remain unclear.
methodsThe cross-disciplinary study, including in vivo, in vitro, and human studies was conducted to explore the cross-talk between proximal tubular epithelial cells (PTECs) and mesangial cells (MCs) in DN. We purified exosome from PTECs treated with high glucose and db/db mice and assessed their influences in the pathologic change of MCs and downstream signal pathway. Healthy individuals and type 2 diabetic patients were enrolled to examine the role of exosomes in clinical applications.
resultsHigh glucose stimulated PTECs to secrete exosomal miR-92a-1-5p, which was taken-up by glomerular MCs, inducing myofibroblast transdifferentiation (MFT) in vitro and in vivo. PTEC-released exosomal 92a-1-5p decreased reticulocalbin-3 expression, leading to endoplasmic reticulum (ER) stress by downregulating genes essential for ER homeostasis including calreticulin and mesencephalic astrocyte-derived neurotrophic factor. Treatment with miR-92a-1-5p inhibitor ameliorated kidney damage in db/db mice with DN. Urinary miR-92a-1-5p could predict kidney injury in type 2 diabetic patients.
conclusionsPTEC-derived exosomal miR-92a-1-5p modulated the kidney microenvironment in vivo and in vitro models, which altered ER stress and MFT in MCs resulting in DN progression. Further blocking miR-92a-1-5p epigenetic regulatory network could be a potential therapeutic strategy to prevent the progression of DN. Video Abstract.
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