ArticlePloS one2021
Recombinant apoptosis inhibitor of macrophage protein reduces delayed graft function in a murine model of kidney transplantation.
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 10 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Prediction models for infection after kidney transplantation: a systematic review.Frontiers in medicine · 2026Pooled it
- A kidney-protective mechanism via cellular oxidative stress reduction induced by CD5L protein.Cell death discovery · 2026Article
- The role of an anti-inflammatory molecule AIM/CD5L in gut ischemia/reperfusion injury of male mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- Macrophage regulated cell death: implications and mechanisms in organ transplantation.Frontiers in immunology · 2025Review
- The effects of apoptosis inhibitor of macrophage in kidney diseases.European journal of medical research · 2024Review
- The comprehensive role of apoptosis inhibitor of macrophage (AIM) in pathological conditions.Clinical and experimental immunology · 2023Review
- Multiple Shades of Gray-Macrophages in Acute Allograft Rejection.International journal of molecular sciences · 2023Review
- Balancing the View of C1q in Transplantation: Consideration of the Beneficial and Detrimental Aspects.Frontiers in immunology · 2022Article
- New therapeutic concepts against ischemia-reperfusion injury in organ transplantation.Expert review of clinical immunologyReview
- 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
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Reperfusion injury following cold and warm ischemia (IRI) is unavoidable during kidney transplantation and contributes to delayed graft function (DGF) and premature graft loss. Death of tubular epithelial cells (TECs) by necrosis during IRI releases pro-inflammatory mediators (e.g. HMGB1), propagating further inflammation (necroinflammation) and tissue damage. Kidney Injury Molecule-1 (KIM-1) is a phagocytic receptor upregulated on proximal TECs during acute kidney injury. We have previously shown that renal KIM-1 protects the graft against transplant associated IRI by enabling TECs to clear apoptotic and necrotic cells, and that recognition of necrotic cells by KIM-1 is augmented in the presence of the opsonin, apoptosis inhibitor of macrophages (AIM). Here, we tested whether recombinant AIM (rAIM) could be used to mitigate transplant associated IRI. We administered rAIM or vehicle control to nephrectomised B6 mice transplanted with a single B6 donor kidney. Compared to grafts in vehicle-treated recipients, grafts from rAIM-treated mice exhibited significantly less renal dysfunction, tubular cell death, tissue damage, tubular obstruction, as well as local and systemic inflammation. Both mouse and human rAIM enhanced the clearance of necrotic cells by murine and human TECs, respectively in vitro. These data support testing of rAIM as a potential therapeutic agent to reduce DGF following kidney transplantation.
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Registered trials
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