ArticleArchivum immunologiae et therapiae experimentalis2022
CD5L Secreted by Macrophage on Atherosclerosis Progression Based on Lipid Metabolism Induced Inflammatory Damage.
Article in Archivum immunologiae et therapiae experimentalis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Exosome-delivered bioactive molecules regulate macrophage polarization in atherosclerosis and myocardial infarction: mechanisms and therapeutic potential.Frontiers in cardiovascular medicine · 2026Review
- The role of exosomes in immunopathology and potential therapeutic implications.Cellular & molecular immunology · 2025Review
- Macrophage-driven exosomes regulate the progression of cardiovascular disease.Frontiers in pharmacology · 2025Review
- Metabolic Activity in Human Intermuscular Adipose Tissue Directs the Response of Resident PPARγBiomedicines · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To explore the molecular mechanism of exosomal protein CD5L secreted by macrophage to promote the progression of atherosclerosis. Twenty cases of patients with atherosclerosis (AS) and 20 cases of healthy subjects were collected. Morphological properties of exosomes were identified by transmission electron microscopy, and the marker proteins CD63 and CD81 of exosomes were measured by Western blot. The secretion of inflammatory factors in the blood supernatant were analyzed by ELISA. Atherosclerosis cell models were established by transwell and separated into three groups: first group was treated with exosome inhibitor (GW4869), second group was injected with CD5L protein and third group was model control. Morphological properties of exosomes were identified by transmission electron microscopy, and the marker proteins CD63 and CD81 of exosomes were measured by Western blot. The levels of TNF-α, IL-1β, IL-6, IL-13, IL-17A, IL-31 in the cells were analyzed by ELISA. Analysis of the expression and distribution of IL-17RA in vascular smooth muscle cells by immunofluorescence. The proteins of CD63, CD81, CD5L were high expressed in AS group compared to healthy subject group. Cell test results showed that protein levels of CD63, CD81, CD5L in AS group were much higher than that in normal group. Immunofluorescence showed that the expression level of IL-17RA in cell membrane was the highest in the AS model group, and the expression of IL-17RA was decreased in GW4869 group and CD5L group. Expression of inflammatory factors in AS was much higher than that in GW4869 group and CD5L group. The exosomal protein CD5L secreted by macrophage promotes the development of atherosclerosis based on lipid metabolism-induced inflammatory damage of vascular smooth muscle cells.
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Registered trials
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