ArticleMediators of inflammation2024
Macrophages Promote Atherosclerosis Development by Inhibiting CD8T Cell Apoptosis.
Article in Mediators of inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Identification and verification of diagnostic biomarkers related to endoplasmic reticulum stress for atherosclerosis.BMC cardiovascular disorders · 2026Article
- Role of solute carrier family 7 member 7 in cancer: opportunities for tumor microenvironment research.Journal for immunotherapy of cancer · 2026Review
- Vascular smooth muscle cell RNA-binding protein U2AF2 induces copper death by regulating C1qbp expression, delaying development of atherosclerosise.Biological research · 2026Article
- SLC4A10 impedes atherosclerosis by diminishing IFN-γ/GZMB levels of CD8Frontiers in immunology · 2025Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atherosclerosis is an inflammatory cardiovascular disease. However, whether the association of immune cells in plaques promotes the progression of this disease has not yet been completely elucidated. Materials and Methods: Thus, this study aimed to investigate the relationship between C1q+ macrophages and CD8T cells through scRNA-seq data reanalysis, quantitative real-time PCR, and flow cytometry. Chromatin immunoprecipitation-quantitative polymerase chain reaction, western blot, and antibody-blocking experiments were performed to investigate the role of macrophage-CD8T interaction in atherosclerosis. An atherosclerotic mouse model was developed to confirm our findings. Results: Mechanistically, Spi1 expression induced by granulocyte-macrophage colony-stimulating factor promoted C1q expression in the macrophages. Moreover, C1q+ macrophages suppressed CD8T cell apoptosis by upregulating Slc7a7 expression to enhance the L-arginine uptake of CD8T cells. CD8T-derived interferon- Conclusion: In conclusion, macrophages interacting with CD8T promote atherosclerosis development via the C1q-C1qbp axis.
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