ArticleCell & bioscience2023
Macrophage-derived exosomes mediate glomerular endothelial cell dysfunction in sepsis-associated acute kidney injury.
Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 26 citations in OpenAlex.
- Curcumin regulates ferroptosis by activating α7 nicotinic acetylcholine receptor to improve sepsis-induced acute kidney injury.Renal failure · 2026Article
- Mapping the knowledge landscape and identifying frontiers of mitochondrial dysfunction in sepsis-associated acute kidney injury: a four-decade bibliometric and visualized analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Role of mitochondria-associated ER membranes in lipid metabolism: implications for renal lipotoxicity.Bioscience reports · 2026Review
- Immune molecular mechanisms of PANoptosis in sepsis-induced acute kidney injury.Inflammation and regeneration · 2026Review
- A macrophage-endothelial cell axis in kidney diseases.International urology and nephrology · 2026Review
- Extracellular vesicles mediate immune regulation in acute kidney injury.Frontiers in immunology · 2026Review
- Macrophage-derived exosomes carrying miR-30a-5p alleviates IL-13/IL4-induced epithelial-mesenchymal transition in mouse bronchial epithelial cells via Runx1.BMC pulmonary medicine · 2025Article
- The aggregate index of systemic inflammation is positively correlated with the risk of all-cause mortality in sepsis-associated acute kidney injury.Scientific reports · 2025Article
- Exosomes applications in kidney diseases.Molecular biology reports · 2025Review
- Emerging Frontiers in acute kidney injury: The role of extracellular vesicles.Bioactive materials · 2025Review
- Mechanisms of Acute Kidney Injury-Chronic Kidney Disease Transition: Unraveling Maladaptive Repair and Therapeutic Opportunities.Biomolecules · 2025Review
- Extracellular Vesicles in Renal Inflammatory Diseases: Revealing Mechanisms of Extracellular Vesicle-Mediated Macrophage Regulation.International journal of molecular sciences · 2025Review
- Monocyte-macrophage membrane expression of IL-1R2 is a severity biomarker in sepsis.Cell death & disease · 2025Article
- Emerging roles of exosomes in the diagnosis and treatment of kidney diseases.Frontiers in pharmacology · 2025Review
- Urinary exosomes as promising biomarkers for early kidney disease detection.American journal of clinical and experimental urology · 2025Review
- Extracellular Vesicles in Acute Kidney Injury: Mechanisms, Biomarkers, and Therapeutic Potential.International journal of nanomedicine · 2025Review
- Serum Exosomes miR-122-5P Induces Hepatic and Renal Injury in Septic Rats by Regulating TAK1/SIRT1 Pathway.Infection and drug resistance · 2025Article
- Exosomes on the development and progression of renal fibrosis.Cell proliferation · 2024Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundSepsis-associated AKI has been shown to be related to sepsis mortality. Macrophage activation and endothelial cell damage are involved in the progression of sepsis-associated AKI, but the specific mechanisms are still unclear.
methodsIn vitro experiments, exosomes extracted from lipopolysaccharide (LPS) -stimulated macrophages were co-incubated with rat glomerular endothelial cells (RGECs) and then detected the injury markers of RGECs. Acid sphingomyelinase (ASM) inhibitor amitriptyline were used to investigate the role of ASM. In vivo experiment, exosomes produced by LPS-stimulated macrophages were injected into mice through tail vein to further explore the role of macrophage-derived exosomes. Moreover, ASM knockout mice were used to verify the mechanism.
resultIn vitro, the secretion of macrophage exosomes increased upon the stimulation with LPS. Notably, macrophage-derived exosomes can cause glomerular endothelial cell dysfunction. In vivo, macrophage infiltration and exosome secretion in glomeruli of the LPS-induced AKI group increased. The exosomes produced by LPS-stimulated macrophages were injected into mice, which also led to the injury of renal endothelial cells. In addition, in the LPS-induced AKI mouse model, compared with wild-type mice, the secretion of exosomes in glomeruli of ASM gene knockout mice and the injury of endothelial cells were reduced.
conclusionOur study shows that ASM regulates the secretion of macrophage exosomes, leading to endothelial cell injury, which may be a therapeutic target in sepsis-associated AKI.
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