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Trem2 promotes foamy macrophage lipid uptake and survival in atherosclerosis
Patterson MT, Firulyova MM, Xu Y, Hillman H, Bishop C, Zhu A, Hickok GH, Schrank PR et al.. Nature cardiovascular research, 2023-10-30
Topic: Brain proteins, microglia and lab models
Atherosclerosis is driven by the expansion of cholesterol-loaded 'foamy' macrophages in the arterial intima. Factors regulating foamy macrophage differentiation and survival in plaque remain poorly understood. Here we show, using trajectory analysis of integrated single-cell RNA sequencing data and a genome-wide CRISPR screen, that triggering receptor expressed on myeloid cells 2 (Trem2) is associated with foamy macrophage specification.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Patterson, M. T., Firulyova, M. M., Xu, Y., Hillman, H., Bishop, C., Zhu, A., et al. (2023). Trem2 promotes foamy macrophage lipid uptake and survival in atherosclerosis. Nature cardiovascular research. https://doi.org/10.1038/s44161-023-00354-3
Vancouver
Patterson MT, Firulyova MM, Xu Y, Hillman H, Bishop C, Zhu A, et al. Trem2 promotes foamy macrophage lipid uptake and survival in atherosclerosis. Nature cardiovascular research. 2023. doi:10.1038/s44161-023-00354-3. PMID: 38646596.
BibTeX
@article{patterson2023-38646596,
author = {Patterson, M. T. and Firulyova, M. M. and Xu, Y. and Hillman, H. and Bishop, C. and Zhu, A. and Hickok, G. H. and Schrank, P. R. and others},
title = {{Trem2 promotes foamy macrophage lipid uptake and survival in atherosclerosis}},
journal = {Nature cardiovascular research},
year = {2023},
doi = {10.1038/s44161-023-00354-3},
pmid = {38646596},
url = {https://doi.org/10.1038/s44161-023-00354-3}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- Factors regulating foamy macrophage differentiation and survival in plaque remain poorly understood.
- Here we show, using trajectory analysis of integrated single-cell RNA sequencing data and a genome-wide CRISPR screen, that triggering receptor expressed on myeloid cells 2 (Trem2) is associated with foamy macrophage specification.
- Loss of Trem2 led to a reduced ability of foamy macrophages to take up oxidized low-density lipoprotein (oxLDL).
- Myeloid-specific deletion of Trem2 showed an attenuation of plaque progression, even when targeted in established atherosclerotic lesions, and was independent of changes in circulating cytokines, monocyte recruitment or cholesterol levels.
Why it matters
This study is about atherosclerosis and shows that Trem2 is associated with foamy macrophage specification, with loss of Trem2 reducing the ability of foamy macrophages to take up oxidized low-density lipoprotein. It concerns plaque macrophages in arteries, not Alzheimer's disease, and provides no direct information about treating, curing or preventing Alzheimer's.
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Study details
- Evidence strengthLow
How this study scored 50/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Nature cardiovascular research) |
| Journal's citation record | 0 / 4 | Nature Cardiovascular Research: journal h-index 58 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 3 / 5 | 2023 — within 6 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 179 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 35.8 citations a year over 5 year(s) since 2023 |
| Impact for its field and year | 4 / 6 | Cited 15.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 other studies in this library |
| Still being cited | 3 / 4 | Cited 175 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Jesse W. Williams: h-index 42 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Centre National de la Recherche Scientifique: institution h-index 2,511 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 8 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 38646596) |
| Free to read | 2 / 2 | Free to read |
| Total | 50 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1038/s44161-023-00354-3
- PubMed: 38646596
- Original source →
- Free full text: Nature Cardiovascular Research →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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