ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Macrophage HM13/SPP Enhances Foamy Macrophage Formation and Atherogenesis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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Who cites it
4 citing papers in PubMed.
- Copper-Doped Prussian Blue Nanozymes With Hyaluronic Acid-Mediated Targeting Alleviate Oxidative Stress and Regulate Cholesterol Handling for Atherosclerosis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Inferring genetic associations of programmed cell death genes with retinitis pigmentosa through multimodal Mendelian randomization.Molecular medicine (Cambridge, Mass.) · 2026Article
- Elemene Augments the Effects of Anti-PD-1 Immunotherapy on Hepatocellular Carcinoma by Regulating the miR-130a-5p/SPP/MHC-I Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Macrophage HM13/SPP Enhances Foamy Macrophage Formation and Atherogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Aryl Hydrocarbon Receptor-Interacting Protein (AIP) reduces macrophage cholesterol-ester accumulation and may prevent atherogenic foamy macrophage formation. Analyzing AIP-associated regulatory gene networks can aid in identifying key regulatory mechanism(s) underlying foamy macrophage formation. A weighted gene co-expression network analysis on the Stockholm Atherosclerosis Gene Expression (STAGE) patient cohort identifies AIP as a negative correlate of Histocompatibility Minor 13 (HM13), which encodes the ER-associated degradation (ERAD) protein Signal Peptide Peptidase (HM13/SPP). The negative correlation between AIP and HM13/SPP on mRNA and protein levels is validated in oxLDL-stimulated macrophages and human plaque foamy macrophages. Mechanistically, AIP, via its chaperone interaction with Aryl Hydrocarbon Receptor (AHR), inhibits p38-c-JUN-mediated HM13 transactivation, thereby suppressing macrophage lipid accumulation. Myeloid HM13/SPP overexpression enhances oxLDL-induced foamy macrophage formation in vitro as well as atherogenesis and plaque foamy macrophage load in vivo, while myeloid HM13/SPP knockout produces the opposite effects. Mechanistically, myeloid HM13/SPP enhances oxLDL-induced foamy macrophage formation in vitro as well as atherogenesis and plaque foamy macrophage load in vivo via promoting ERAD-mediated proteasomal degradation of the metabolic regulator Heme Oxygenase-1 (HO-1). In conclusion, AIP downregulates macrophage HM13/SPP, a driver of oxLDL-induced lipid loading, foamy macrophage generation, and atherogenesis.
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Registered trials
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