ArticleCell death & disease2021
SAP130 released by damaged tubule drives necroinflammation via miRNA-219c/Mincle signaling in acute kidney injury.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Research hotspots and future trends in sepsis-associated acute kidney injury: a bibliometric and visualization analysis.Frontiers in medicine · 2024Pooled it
- C-type lectin receptors: bone remodeling and therapeutic potential.Bone research · 2026Review
- Review
- D4F-Functionalized Ceria Nanozyme-CasRx Platform Suppresses STING and Reprograms the Renal Immune Niche in Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophages as tissue scavengers, builders, and sensors.Function (Oxford, England) · 2026Review
- LncRNA H19 overexpression protects against acute kidney injury after cardiopulmonary bypass via activating Pink1/Parkin-mediated mitophagy.Chinese medical journal · 2026Article
- Unravelling mechanisms regulating Mincle activation.Communications biology · 2026Review
- Remodeling the tumor immune microenvironment: mechanisms of crosstalk between regulated cell death macrophages.Frontiers in immunology · 2026Review
- Microbiota-associated metabolic networks in gut-kidney communication and renal immune regulation: mechanisms and therapeutic potential.Frontiers in microbiology · 2026Review
- Zileuton Attenuates Acute Kidney Injury in Glycerol-Induced Rhabdomyolysis by Regulating Myeloid-Derived Suppressor Cells in Mice.International journal of molecular sciences · 2025Article
- The spleen tyrosine kinase inhibitor entospletinib resolves inflammation to promote repair following acute kidney injury.JCI insight · 2025Article
- SARS-CoV-2 nucleocapsid protein induces a Mincle-dependent macrophage inflammatory response in acute kidney injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- The SAP130/Mincle axis was involved in sevoflurane-induced neuronal death and microglial activation in juvenile mice.Frontiers in pharmacology · 2025Article
- Role of miRNAs in macrophage-mediated kidney injury.Pediatric nephrology (Berlin, Germany) · 2024Review
- DAMP sensing and sterile inflammation: intracellular, intercellular and inter-organ pathways.Nature reviews. Immunology · 2024Review
- Identification of a Novel ECM Remodeling Macrophage Subset in AKI to CKD Transition by Integrative Spatial and Single-Cell Analysis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Landscape of peripheral immunity in patients with upper urinary tract urolithiasis and the underlying correlations with renal function.BMC urology · 2024Article
- Mincle as a potential intervention target for the prevention of inflammation and fibrosis (Review).Molecular medicine reports · 2024Review
- Mincle receptor in macrophage and neutrophil contributes to the unresolved inflammation during the transition from acute kidney injury to chronic kidney disease.Frontiers in immunology · 2024Article
- HYAL1 deficiency attenuates lipopolysaccharide-triggered renal injury and endothelial glycocalyx breakdown in septic AKI in mice.Renal failure · 2023Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Tubules injury and immune cell activation are the common pathogenic mechanisms in acute kidney injury (AKI). However, the exact modes of immune cell activation following tubule damage are not fully understood. Here we uncovered that the release of cytoplasmic spliceosome associated protein 130 (SAP130) from the damaged tubular cells mediated necroinflammation by triggering macrophage activation via miRNA-219c(miR-219c)/Mincle-dependent mechanism in unilateral ureteral obstruction (UUO) and cisplatin-induced AKI mouse models, and in patients with acute tubule necrosis (ATN). In the AKI kidneys, we found that Mincle expression was tightly correlated to the necrotic tubular epithelial cells (TECs) with higher expression of SAP130, a damaged associated molecule pattern (DAMP), suggesting that SAP130 released from damaged tubular cells may trigger macrophage activation and necroinflammation. This was confirmed in vivo in which administration of SAP130-rich supernatant from dead TECs or recombinant SAP130 promoted Mincle expression and macrophage accumulation which became worsen with profound tubulointerstitial inflammation in LPS-primed Mincle WT mice but not in Mincle deficient mice. Further studies identified that Mincle was negatively regulated via miR-219c-3p in macrophages as miR-219c-3p bound Mincle 3'-UTR to inhibit Mincle translation. Besides, lentivirus-mediated renal miR-219c-3p overexpression blunted Mincle and proinflammatory cytokine expression as well as macrophage infiltration in the inflamed kidney of UUO mice. In conclusion, SAP130 is released by damaged tubules which elicit Mincle activation on macrophages and renal necroinflammation via the miR-219c-3p-dependent mechanism. Results from this study suggest that targeting miR-219c-3p/Mincle signaling may represent a novel therapy for AKI.
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Registered trials
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