ArticleThe Journal of experimental medicine2020
C-type lectin Mincle mediates cell death-triggered inflammation in acute kidney injury.
Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 56 citations in OpenAlex.
- Transcriptome and weighted gene co-expression network analysis identify hub genes and pathways in rat kidneys after deep hypothermic circulatory arrest.Renal failure · 2026Article
- C-type lectin receptors: bone remodeling and therapeutic potential.Bone research · 2026Review
- Review
- Mechanisms of regeneration and maladaptive repair in acute kidney injury.Nature reviews. Nephrology · 2026Review
- C-Type lectin receptors as key modulators of intestinal inflammation: insights into IBD pathogenesis and therapy.FEMS microbiology letters · 2026Review
- Altered glycolipid metabolism during acute kidney injury exacerbates renal inflammation.Scientific reports · 2025Article
- The spleen tyrosine kinase inhibitor entospletinib resolves inflammation to promote repair following acute kidney injury.JCI insight · 2025Article
- Novel Cell-to-Cell Communications Between Macrophages and Fibroblasts Regulate Obesity-Induced Adipose Tissue Fibrosis.Diabetes · 2025Article
- Substrates, regulation, cellular functions, and disease associations of P4-ATPases.Communications biology · 2025Review
- Small extracellular vesicles from human umbilical cord mesenchymal stem cells delivering miR-202-5p alleviate renal ischemia-reperfusion injury by targeting the GOLIM4/PI3K/AKT axis.Frontiers in immunology · 2025Article
- The multifaceted role of macrophages in kidney physiology and diseases.Frontiers in immunology · 2025Review
- 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
- Engineered Cancer Nanovaccines: A New Frontier in Cancer Therapy.Nano-micro letters · 2024Review
- Mincle as a potential intervention target for the prevention of inflammation and fibrosis (Review).Molecular medicine reports · 2024Review
- Glucosylceramide flippases contribute to cellular glucosylceramide homeostasis.Journal of lipid research · 2024Article
- Transcriptomic analysis ofFrontiers in veterinary science · 2024Article
- 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
- Infiltrating myeloid cell-derived properdin markedly promotes microglia-mediated neuroinflammation after ischemic stroke.Journal of neuroinflammation · 2023Article
- Acute systemic myeloid inflammatory and stress response in severe food allergic reactions.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2023Article
- Macrophages mediate psoriasis via Mincle-dependent mechanism in mice.Cell death discovery · 2023Article
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence indicates that cell death triggers sterile inflammation and that impaired clearance of dead cells causes nonresolving inflammation; however, the underlying mechanisms are still unclear. Here, we show that macrophage-inducible C-type lectin (Mincle) senses renal tubular cell death to induce sustained inflammation after acute kidney injury in mice. Mincle-deficient mice were protected against tissue damage and subsequent atrophy of the kidney after ischemia-reperfusion injury. Using lipophilic extract from the injured kidney, we identified β-glucosylceramide as an endogenous Mincle ligand. Notably, free cholesterol markedly enhanced the agonistic effect of β-glucosylceramide on Mincle. Moreover, β-glucosylceramide and free cholesterol accumulated in dead renal tubules in proximity to Mincle-expressing macrophages, where Mincle was supposed to inhibit clearance of dead cells and increase proinflammatory cytokine production. This study demonstrates that β-glucosylceramide in combination with free cholesterol acts on Mincle as an endogenous ligand to induce cell death-triggered, sustained inflammation after acute kidney injury.
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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.