ArticleNature medicine2016
Apoptosis inhibitor of macrophage protein enhances intraluminal debris clearance and ameliorates acute kidney injury in mice.
Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.
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Who cites it
117 citing papers in PubMed, 1 synthesis or guideline pooled it, 222 citations in OpenAlex.
- Recent Progression and Treatment Approaches for the Kidney Stone Management.Current drug targets · 2025Pooled it
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- Proteomic and Transcriptomic Signatures of Poor Asthma Symptom Control in the U-BIOPRED Cohort.Allergy · 2026Article
- The Berberine Derivative BBR684 Inhibits VDAC Oligomerization to Suppress Ferroptosis in Acute Kidney Injury.Current therapeutic research, clinical and experimental · 2026Article
- A kidney-protective mechanism via cellular oxidative stress reduction induced by CD5L protein.Cell death discovery · 2026Article
- Prevalence of theJournal of feline medicine and surgery · 2026Article
- CD5L promotes efferocytosis and resolution of retinal ischemic injury.Cell death & disease · 2026Article
- CD5L insufficiency exacerbates skeletal joint damage in rheumatoid arthritis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Serum antithrombin III level predicts acute kidney injury in patients with traumatic brain injury.Experimental and therapeutic medicine · 2026Article
- FAR1 as a ferroptosis-related biomarker and potential therapeutic target in acute kidney injury: integrated bioinformatics and experimental validation.Renal failure · 2025Article
- The role of an anti-inflammatory molecule AIM/CD5L in gut ischemia/reperfusion injury of male mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- Variation in virion phosphatidylserine content drives differential GAS6 binding among closely related flaviviruses.Journal of virology · 2025Article
- Apoptosis Inhibitor of Macrophage (AIM) Modulates Calcium Oxalate-Induced Ureteral Fibrosis in AIM-Felinized Mice.International journal of molecular sciences · 2025Article
- Innate immune responses to lysosomal nucleic acid stress.Journal of biochemistry · 2025Review
- RNase T2 deficiency promotes TLR13-dependent replenishment of tissue-protective Kupffer cells.The Journal of experimental medicine · 2025Article
- Release of apoptosis inhibitor of macrophage (AIM) from pentameric IgM in serum predicts prognosis after hemodialysis initiation.Communications medicine · 2025Article
- Gas6 induces AIM to suppress acute lung injury in mice by inhibiting NLRP3 inflammasome activation and inducing autophagy.Frontiers in immunology · 2025Article
- Apoptosis inhibitor of macrophage suppress immune responses via IL-10 production and delay bacterial clearance inFrontiers in cellular and infection microbiology · 2025Article
- Scavenger receptors: key players in the immunological puzzle of lupus.Frontiers in lupus · 2025Article
57 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 7 institutions in 2 countries.
Funding
Abstract
Acute kidney injury (AKI) is associated with prolonged hospitalization and high mortality, and it predisposes individuals to chronic kidney disease. To date, no effective AKI treatments have been established. Here we show that the apoptosis inhibitor of macrophage (AIM) protein on intraluminal debris interacts with kidney injury molecule (KIM)-1 and promotes recovery from AKI. During AKI, the concentration of AIM increases in the urine, and AIM accumulates on necrotic cell debris within the kidney proximal tubules. The AIM present in this cellular debris binds to KIM-1, which is expressed on injured tubular epithelial cells, and enhances the phagocytic removal of the debris by the epithelial cells, thus contributing to kidney tissue repair. When subjected to ischemia-reperfusion (IR)-induced AKI, AIM-deficient mice exhibited abrogated debris clearance and persistent renal inflammation, resulting in higher mortality than wild-type (WT) mice due to progressive renal dysfunction. Treatment of mice with IR-induced AKI using recombinant AIM resulted in the removal of the debris, thereby ameliorating renal pathology. We observed this effect in both AIM-deficient and WT mice, but not in KIM-1-deficient mice. Our findings provide a basis for the development of potentially novel therapies for 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.