ArticleMolecular biomedicine2025
ER stress induced extracellular vesicles secretion from macrophages promotes calcium oxalate crystals formation in kidney.
Article in Molecular biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Extracts ofPharmaceuticals (Basel, Switzerland) · 2026Article
- PTGIS inhibited osteogenic and promoted angiogenic differentiation of bone marrow mesenchymal stem cells via endoplasmic reticulum stress mediated PI3K/AKT signaling.Stem cell research & therapy · 2026Article
- Interaction between transient receptor potential vanilloid 4 and glutamate NMDA receptor subunit 1 mediates endoplasmic reticulum stress and neuroinflammation in postoperative delirium.Molecular biomedicine · 2026Article
- The Application of Nanomaterials in Kidney Stone Disease: Emerging Strategies for Early Diagnosis, Targeted Therapy, and Prevention.International journal of nanomedicine · 2026Review
- Cross-Species Identification of Urinary Small Extracellular Vesicle-Associated miR-223-3p as a Candidate Biomarker for Nephrolithiasis in a Discovery Cohort.International journal of medical sciences · 2026Article
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Authors and funding
6 authors.
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Abstract
Macrophages are involved in the development of kidney stone disease, and substantial research suggests that macrophage-derived extracellulr vesicles (Mφ-EVs) may play a pivotal role in this process. However, the impact of Mφ-EVs on kidney stone formation and the mechanisms of EVs secretion remain unclear. Here we found that calcium oxalate (CaOx) crystals stimulation leads to increased inflammation and enhanced secretion of extracellular vesicles (EVs) in macrophages. Interestingly, these EVs can be absorbed by renal cells, significantly promoting renal tubular damage and facilitating the formation of CaOx crystals in mouse kidneys. Mechanistically, CaOx crystal stimulation activates endoplasmic reticulum stress (ERS)-related proteins, particularly PKR-like ER kinase (PERK), resulting in the production of EVs containing glucose-regulated protein 94 (GRP94). Concurrently, this process induces lysosomal dysfunction, inhibiting the degradation of EVs by lysosomes and ultimately leading to their release. Knocking down PERK in macrophages could reduce the Mφ-EVs secretion significantly, which decreased in the accumulation of CaOx crystals in the mouse kidneys. Together, our research uncovers a novel mechanism by which CaOx crystal-induced ERS and lysosomal dysfunction in macrophages promote the secretion of EVs, thereby facilitating kidney stone formation. This finding presents a promising therapeutic target for future interventions.
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