ArticleJCI insight2022
JAML promotes acute kidney injury mainly through a macrophage-dependent mechanism.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 51 citations in OpenAlex.
- GABA ameliorates diabetic kidney disease-induced podocyte injury via JAML-FPR2 axis-mediated suppression of macrophage infiltration.Renal failure · 2026Article
- TREM2 in Macrophages Promotes Renal Fibrosis via Activation of β-Catenin Signalling Pathway in Obstructive Nephropathy.Cell proliferation · 2026Article
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- A pH-responsive ultrasmall Fe-kaempferol nanoplatform ameliorates acute kidney injury by enhancing efferocytosis and metabolic reprogramming.Journal of nanobiotechnology · 2026Article
- Dynamic regulation and targeted interventions of macrophages in ischemia-reperfusion injury.Journal of advanced research · 2026Review
- Multi-omics and machine learning reveal LYZ and ISG15 as diagnostic and therapeutic targets in autoimmune-mediated chronic kidney disease.Frontiers in immunology · 2026Article
- Targeting efferocytosis for tissue regeneration: From microenvironment reprogramming to clinical translation.Theranostics · 2026Review
- Elimination of Senescent Macrophages by Purinergic Receptor P2RX7 Antagonist to Safeguard Against Kidney Injury and Aging.International journal of biological sciences · 2026Article
- Multi-omics mapping of PSC genetic risk to a high TWAS-active JAML+ lipid-associated macrophage program: bridging single-cell heterogeneity, spatial fibrotic niches, and machine learning selection.Frontiers in cell and developmental biology · 2026Article
- Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney.Life (Basel, Switzerland) · 2025Review
- Piezo1 aggravates ischemia/reperfusion-induced acute kidney injury by CaRenal failure · 2025Article
- An atlas of ferroptosis-induced secretomes.Cell death and differentiation · 2025Article
- Macrophage junctional adhesion molecule-like (JAML) protein promotes NLRP3 inflammasome activation in the development of atherosclerosis.Cell death and differentiation · 2025Article
- Acute kidney injury: pathogenesis and therapeutic interventions.Molecular biomedicine · 2025Review
- Overexpression of JAML in colorectal cancer cells predicts higher radiosensitivity by inactivating ATR pathway.Clinical and translational radiation oncology · 2025Article
- Associations between serum JAML, nesfatin-1, and 25(OH)D and the risk of diabetic kidney disease in patients with type 2 diabetes.Scientific reports · 2025Article
- Renal tubular GSDME protects cisplatin nephrotoxicity by impeding OGT-STAT3-S100A7A axis in male mice.Nature communications · 2025Article
- Ablation of macrophage transcriptional factor FoxO1 protects against ischemia-reperfusion injury-induced acute kidney injury.Acta pharmaceutica Sinica. B · 2025Article
- Article
- Therapeutic role of hucMSC-sEV-enriched miR-13896 in cisplatin-induced acute kidney injury through M2 macrophage polarization.Cell biology and toxicology · 2025Article
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although macrophages are undoubtedly attractive therapeutic targets for acute kidney injury (AKI) because of their critical roles in renal inflammation and repair, the underlying mechanisms of macrophage phenotype switching and efferocytosis in the regulation of inflammatory responses during AKI are still largely unclear. The present study elucidated the role of junctional adhesion molecule-like protein (JAML) in the pathogenesis of AKI. We found that JAML was significantly upregulated in kidneys from 2 different murine AKI models including renal ischemia/reperfusion injury (IRI) and cisplatin-induced AKI. By generation of bone marrow chimeric mice, macrophage-specific and tubular cell-specific Jaml conditional knockout mice, we demonstrated JAML promoted AKI mainly via a macrophage-dependent mechanism and found that JAML-mediated macrophage phenotype polarization and efferocytosis is one of the critical signal transduction pathways linking inflammatory responses to AKI. Mechanistically, the effects of JAML on the regulation of macrophages were, at least in part, associated with a macrophage-inducible C-type lectin-dependent mechanism. Collectively, our studies explore for the first time to our knowledge new biological functions of JAML in macrophages and conclude that JAML is an important mediator and biomarker of AKI. Pharmacological targeting of JAML-mediated signaling pathways at multiple levels may provide a novel therapeutic strategy for patients with AKI.
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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.