ArticleAtherosclerosis2019
Allograft inflammatory factor-1 supports macrophage survival and efferocytosis and limits necrosis in atherosclerotic plaques.
Article in Atherosclerosis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
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- Exercise suppresses breast cancer and reprograms the immune tumor microenvironment, cancer cell intrinsic features, and their interaction.Journal of sport and health science · 2026Article
- Iba1 deficiency impairs microglial synaptic remodeling and neuronal survival after axonal injury.Journal of neuroinflammation · 2026Article
- Hyperglycemia- induced innate immune tolerance involves the metabolic and epigenetic rewiring in human alveolar macrophages.Frontiers in immunology · 2026Article
- The multifaceted role of AIF-1 in metabolic dysregulation: bridging inflammation, insulin resistance, and obesity.Frontiers in endocrinology · 2026Review
- Macrophage-like smooth muscle cells in atherosclerosis.Molecular biology reports · 2025Review
- Rapid manufacturing of angiogenic cellular collagen patches for ischemic cardiomyopathy.Stem cells translational medicine · 2025Article
- Immunization induces inflammation in the mouse heart during spaceflight.BMC genomics · 2025Article
- Mechanical regulation of macrophage metabolism by allograft inflammatory factor 1 leads to adverse remodeling after cardiac injury.Nature cardiovascular research · 2025Article
- Identification of novel protein biomarkers and therapeutic targets for ankylosing spondylitis using human circulating plasma proteomics and genome analysis.Analytical and bioanalytical chemistry · 2024Article
- Identification of allograft inflammatory factor-1 suppressing the progression and indicating good prognosis of osteosarcoma.BMC musculoskeletal disorders · 2024Article
- Identification of key biomarkers for predicting CAD progression in inflammatory bowel disease via machine-learning and bioinformatics strategies.Journal of cellular and molecular medicine · 2024Article
- In silico based analysis to explore genetic linkage between atherosclerosis and its potential risk factors.Biochemistry and biophysics reports · 2023Article
- Review
- Blockade of CD47 function attenuates restenosis by promoting smooth muscle cell efferocytosis and inhibiting their migration and proliferation.The Journal of biological chemistry · 2023Article
- Increased adipose catecholamine levels and protection from obesity with loss of Allograft Inflammatory Factor-1.Nature communications · 2023Article
- Biocompatible Nano-Hydroxyapatites Regulate Macrophage Polarization.Materials (Basel, Switzerland) · 2022Article
- Article
- Monocyte biology conserved across species: Functional insights from cattle.Frontiers in immunology · 2022Article
- Left ventricular assist device bioinformatics identify possible hubgenes and regulatory networks involved in the myocardium of patients with left ventricular assist device.Frontiers in cardiovascular medicine · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND AND
aimsAllograft inflammatory factor-1 (AIF1) has been characterized as a pro-inflammatory molecule expressed primarily in the monocyte/macrophage (MP) lineage and positively associated with various forms of vascular disease, including atherosclerosis. Studies of AIF1 in atherosclerosis have relied on mouse models in which AIF1 was overexpressed in either myeloid or smooth muscle cells, resulting in increased atherosclerotic plaque burden. How physiologic expression of AIF1 contributes to MP biology in atherogenesis is not known.
methodsEffects of global AIF1 deficiency on atherosclerosis were assessed by crossing Aif1
resultsAtherosclerotic plaques in Aif1
conclusionsThese findings characterize AIF1 as a positive regulator of the NF-κB pathway that supports MP functions such as survival and efferocytosis. In inflammatory settings such as atherosclerosis, these AIF1-dependent activities serve to clear cellular and other debris and limit necrotic core expansion, and may oppose lesion destabilization.
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Registered trials
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.