ArticlePloS one2021
High salt exacerbates acute kidney injury by disturbing the activation of CD5L/apoptosis inhibitor of macrophage (AIM) protein.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Recent Progression and Treatment Approaches for the Kidney Stone Management.Current drug targets · 2025Pooled it
- A kidney-protective mechanism via cellular oxidative stress reduction induced by CD5L protein.Cell death discovery · 2026Article
- Plasma Proteomic Profile of Dietary Potassium and Incident CKD.Clinical journal of the American Society of Nephrology : CJASN · 2026Article
- The role of an anti-inflammatory molecule AIM/CD5L in gut ischemia/reperfusion injury of male mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- Apoptosis Inhibitor of Macrophage (AIM) Modulates Calcium Oxalate-Induced Ureteral Fibrosis in AIM-Felinized Mice.International journal of molecular sciences · 2025Article
- Excess dietary sodium restores electrolyte and water homeostasis caused by loss of the endoplasmic reticulum molecular chaperone, GRP170, in the mouse nephron.American journal of physiology. Renal physiology · 2025Article
- A novel model of cardiovascular-kidney-metabolic syndrome combining unilateral nephrectomy and high-salt-sugar-fat diet in mice.Lab animal · 2024Article
- Cryo-EM reveals structural basis for human AIM/CD5L recognition of polymeric immunoglobulin M.Nature communications · 2024Article
- Excess dietary sodium partially restores salt and water homeostasis caused by loss of the endoplasmic reticulum molecular chaperone, GRP170, in the mouse nephron.bioRxiv : the preprint server for biology · 2024Article
- The comprehensive role of apoptosis inhibitor of macrophage (AIM) in pathological conditions.Clinical and experimental immunology · 2023Review
- Sudden Infant Death Syndrome, Pulmonary Edema, and Sodium Toxicity: A Grounded Theory.Diseases (Basel, Switzerland) · 2022Article
- Two independent modes of kidney stone suppression achieved by AIM/CD5L and KIM-1.Communications biology · 2022Article
- Apoptosis Inhibitor of Macrophages in Cats: A Potential Link Between an Exon 3 Variant Allele and Progression of Naturally Occurring Chronic Kidney Disease.Journal of veterinary internal medicineArticle
- Apoptosis Inhibitor of Macrophage (CD5-Like Antigen) in Healthy Dogs and Dogs With Acute Kidney Injury.Journal of veterinary internal medicineArticle
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The influence of excess salt intake on acute kidney injury (AKI) has not been examined precisely except for some clinical data, unlike in chronic kidney disease. Here, we addressed the influence of high salt (HS) on AKI and its underlying mechanisms in terms of the activity of circulating apoptosis inhibitor of macrophage (AIM, also called CD5L) protein, a facilitator of AKI repair. HS loading in mice subjected to ischemia/reperfusion (IR) resulted in high mortality with advanced renal tubular obstruction and marked exacerbation in biomarkers of proximal renal tubular damage. This AKI exacerbation appeared to be caused mainly by the reduced AIM dissociation from IgM pentamer in serum, as IgM-free AIM is indispensable for the removal of intratubular debris to facilitate AKI repair. Injection of recombinant AIM (rAIM) ameliorated the AKI induced by IR/HS, dramatically improving the tubular damage and mouse survival. The repair of lethal AKI by AIM was dependent on AIM/ kidney injury molecule-1 (KIM-1) axis, as rAIM injection was not effective in KIM-1 deficient mice. Our results demonstrate that the inhibition of AIM dissociation from IgM is an important reason for the exacerbation of AKI by HS, that AIM is a strong therapeutic tool for severe 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 Socratic graph.