ArticleNPJ Regenerative medicine2022
Tubular epithelial cells-derived small extracellular vesicle-VEGF-A promotes peritubular capillary repair in ischemic kidney injury.
Article in NPJ Regenerative medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 42 citations in OpenAlex.
- Association between thrombomodulin and the prevalence of renal calculus: a cross-sectional study from Wuhan central hospital.World journal of urology · 2026Article
- T Cell-Independent Role of PD-L1 in Kidney Repair: Mitigation of Tubular DNA Damage via PD-L1/BRCA1 Interaction Following AKI.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tetrahedral framework nucleic acids: Nanokeys unlocking a new era of precision biomedicine.Journal of advanced research · 2026Review
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- Leveraging extracellular vesicle biology for novel tests and therapeutics for kidney fibrosis.Clinical and translational medicine · 2026Review
- A dynamic bioreactor for endothelial and epithelial cell co-culture to mimic aspects of renal microenvironments.Biomedical microdevices · 2026Article
- Shedding light on the role of extracellular vesicles in renal fibrosis.Fundamental research · 2026Review
- The role of the vascular niche in regulating kidney tubulointerstitial fibrosis.Kidney international · 2026Review
- Precision Nanomedicine for Renal Tubular Injury: From Passive Accumulation to Subcellular Targeting.International journal of nanomedicine · 2026Review
- Sema3dInternational journal of biological sciences · 2026Article
- Organ-Specific Extracellular Vesicles in the Treatment of Ischemic Acute Organ Injury: Mechanisms, Successes, and Prospects.International journal of molecular sciences · 2025Review
- Role of metallothionein 3 in diabetic nephropathy via interplay with HIF-1α.Diabetology international · 2025Article
- Single urinary extracellular vesicle proteomics identifies complement receptor CD35 as a biomarker for sepsis-associated acute kidney injury.Nature communications · 2025Article
- Article
- Emerging Frontiers in acute kidney injury: The role of extracellular vesicles.Bioactive materials · 2025Review
- Tubular epithelial cell-derived extracellular vesicles carrying serum amyloid A1 exacerbate sepsis-associated acute kidney injury by promoting NETs formation.Frontiers in immunology · 2025Article
- Glycolysis in Peritubular Endothelial Cells and Microvascular Rarefaction in CKD.Journal of the American Society of Nephrology : JASN · 2025Article
- Purification of mesenchymal stromal cell-derived small extracellular vesicles using ultrafiltration.Journal of extracellular biology · 2025Article
- Molecular mechanisms and therapeutic advances of peritubular capillary neogenesis in acute kidney injury.Frontiers in molecular biosciences · 2025Review
- Specificity of endothelial cells in endothelial dysfunction of diabetic kidney disease and their crosstalk with neighboring cells: an updated review.Frontiers in endocrinology · 2025Review
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Peritubular capillaries (PTCs) are closely related to renal tubules in structure and function, and both are pivotal regulators in the development and progression of acute kidney injury (AKI). However, the mechanisms that underlie the interaction between PTCs and tubules during AKI remain unclear. Here we explored a new mode of tubulovascular crosstalk mediated by small extracellular vesicles (sEV) after AKI. In response to renal ischemia/reperfusion (I/R) injury, endothelial proliferation of PTCs and tubular expression of vascular endothelial growth factor-A (VEGF-A) were increased, accompanied by a remarkable redistribution of cytoplasmic VEGF-A to the basolateral side of tubular cells. Meanwhile, the secretion mode of VEGF-A was converted in the injured tubular cells, which showed a much greater tendency to secrete VEGF-A via sEV other than the free form. Interestingly, tubular cell-derived VEGF-A-enriched sEV (sEV-VEGF-A) turned out to promote endothelial proliferation which was regulated by VEGF receptors 1 and 2. Furthermore, inhibition of renal sEV secretion by Rab27a knockdown resulted in a significant decrease in the proliferation of peritubular endothelial cells in vivo. Importantly, taking advantage of the newly recognized endogenous repair response of PTCs, exogenous supplementation of VEGF-A + sEV efficiently recused PTC rarefaction, improved renal perfusion, and halted the AKI to CKD transition. Taken together, our study uncovered a novel intrinsic repair response after AKI through renal tubule-PTC crosstalk via sEV-VEGF-A, which could be exploited as a promising therapeutic angiogenesis strategy in diseases with ischemia.
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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.