ArticleMolecular therapy : the journal of the American Society of Gene Therapy2023
KIM-1 augments hypoxia-induced tubulointerstitial inflammation through uptake of small extracellular vesicles by tubular epithelial cells.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 49 citations in OpenAlex.
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- 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
- Recent advances in stimuli-responsive nanomaterials for the treatment of acute kidney injury.Journal of nanobiotechnology · 2026Review
- Leveraging extracellular vesicle biology for novel tests and therapeutics for kidney fibrosis.Clinical and translational medicine · 2026Review
- Novel insights into extracellular vesicles: An update on biomolecules, immunomodulation and clinical strategies in skin melanoma.Clinical and translational medicine · 2026Review
- High-Dose Voclosporin Protects Against Acute Kidney Injury via Regnase-2-Mediated NGAL MRNA Decay.International journal of molecular sciences · 2026Article
- Oxidative Stress-Driven Mechanisms and Biomarkers of Drug-Induced Nephrotoxicity: Translational Insights and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- Hypertension-Induced Renal Injury: From Pathophysiology to Therapeutic Perspectives.Biomedicines · 2026Review
- Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026Review
- Shedding light on the role of extracellular vesicles in renal fibrosis.Fundamental research · 2026Review
- Novel Homo-SELEX for selecting universal aptamer for cross-species kidney injury biomarker KIM-1 in muti-scenario situ imaging.Journal of nanobiotechnology · 2026Article
- Molecular mechanisms of acute inflammation: systemic responses and kidney-specific pathophysiology.Function (Oxford, England) · 2026Review
- The double-positive cells in the tumor microenvironment.Journal of translational internal medicine · 2026Article
- Injury-Induced Epithelial Spp1 Engages Cd44 to Promote Neutrophil Recruitment and Exacerbate Acute Kidney Injury.Journal of inflammation research · 2026Article
- Renal-targeted exosomes inhibiting miR-182-5p for treatment of renal ischemia-reperfusion injury.Bioengineering & translational medicine · 2026Article
- Combined dapagliflozin and pioglitazone therapy in diabetic nephropathy: no added benefit beyond monotherapy in inflammation and fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Precision Nanomedicine for Renal Tubular Injury: From Passive Accumulation to Subcellular Targeting.International journal of nanomedicine · 2026Review
- Mild and reversible nephrotoxicity following repeated administration of damnacanthal in nude mice.Toxicology reports · 2025Article
- "Exosomal therapy: a promising approach to alleviate renal dysfunction induced by hypoxia in neonatal seizures".Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
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9 authors at 1 institution in 1 country.
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Abstract
Tubular epithelial cells (TECs) exposed to hypoxia incite tubulointerstitial inflammation (TII), while the exact mechanism is unclear. In this study, we identified that hypoxia evoked tubule injury as evidenced by tubular hypoxia-inducible factor-1α and kidney injury molecule-1 (KIM-1) expression and that renal small extracellular vesicle (sEV) production was increased with the development of TII after ischemia-reperfusion injury (IRI). Intriguingly, KIM-1-positive tubules were surrounded by macrophages and co-localized with sEVs. In vitro, KIM-1 expression and sEV release were increased in hypoxic TECs and the hypoxia-induced inflammatory response was ameliorated when KIM-1 or Rab27a, a master regulator of sEV secretion, was silenced. Furthermore, KIM-1 was identified to mediate hypoxic TEC-derived sEV (Hypo-sEV) uptake by TECs. Phosphatidylserine (PS), a ligand of KIM-1, was present in Hypo-sEVs as detected by nanoflow cytometry. Correspondingly, the inflammatory response induced by exogenous Hypo-sEVs was attenuated when KIM-1 was knocked down. In vivo, exogenous-applied Hypo-sEVs localized to KIM-1-positive tubules and exacerbated TII in IRI mice. Our study demonstrated that KIM-1 expressed by injured tubules mediated sEV uptake via recognizing PS, which participated in the amplification of tubule inflammation induced by hypoxia, leading to the development of TII in ischemic acute kidney injury.
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