ArticleGeroScience2025
Deletion of absent in melanoma-2 (AIM2) drives bone marrow adipogenesis and impairs bone microarchitecture.
Article in GeroScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The Role of the AIM2 Gene in Obesity-Related Glucose and Lipid Metabolic Disorders: A Recent Update.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
Corrections and comments
- Update of
Authors and funding
7 authors.
Funding
Abstract
Absent in melanoma (AIM) 2, a gene induced by interferon, acts as a cytosolic sensor for double-stranded (ds) DNA. It forms the AIM2 inflammasome, producing interleukin (IL)-1β and IL-18. Our previous study demonstrated that mice lacking AIM2 exhibit spontaneous obesity, insulin resistance, and inflammation in adipose tissue. In this study, we aimed to explore the impact of AIM2 gene deletion on the bone marrow microenvironment and bone morphology in adult and aged mice. Utilizing micro-computed tomography (micro-CT), we discovered that female mice lacking AIM2 showed an increase in the total cross-sectional area at 5 months of age, accompanied by an increase in cortical thickness in the mid-diaphysis of the femur at both 5 and 15 months of age. At 15 months, the cortical bone mineral density (BMD) significantly decreased in AIM2 null females compared to wildtype (WT) mice. Trabecular bone volume and BMD at the distal metaphysis of the femur and the lumbar vertebra-4 were also significantly decreased in AIM2 null females. Histological examination of femurs from aged mice demonstrated increased bone marrow adiposity in AIM2 null mice, accompanied by a significant increase in CD45 - /CD31 - /Sca1 + /Pdgfa + adipogenic progenitor cells and a decrease in the ratio of CD45 - /CD31 - /Sca1 - /Pdgfa + osteogenic progenitor cells, as determined by flow cytometry of bone marrow cells. RNAseq analysis of the bone marrow revealed a significant increase in interferon-stimulated genes with Ifi202b as the top-upregulated gene in AIM2 null mice. Our findings suggest that AIM2 deficiency affects bone health by promoting adipogenesis in the bone marrow and inducing a pro-inflammatory environment, thereby contributing to decreased bone mineral density.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.