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TREM2 deficiency aggravates renal injury by promoting macrophage apoptosis and polarization via the JAK-STAT pathway in mice
Cui Y, Chen C, Tang Z, Yuan W, Yue K, Cui P, Qiu X, Zhang H et al.. Cell death & disease, 2024-06-07
Topic: Brain proteins, microglia and lab models
The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor that affects cellular phenotypes by modulating phagocytosis and metabolism, promoting cell survival, and counteracting inflammation. Its role in renal injury, in particular, unilateral ureteral obstruction (UUO) or ischemia-reperfusion injury (IRI)-induced renal injury remains unclear. In our study, WT and Trem2 -/- mice were employed to evaluate the role of TREM2 in renal macrophage infiltration and tissue injury after UUO.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Cui, Y., Chen, C., Tang, Z., Yuan, W., Yue, K., Cui, P., et al. (2024). TREM2 deficiency aggravates renal injury by promoting macrophage apoptosis and polarization via the JAK-STAT pathway in mice. Cell death & disease. https://doi.org/10.1038/s41419-024-06756-w
Vancouver
Cui Y, Chen C, Tang Z, Yuan W, Yue K, Cui P, et al. TREM2 deficiency aggravates renal injury by promoting macrophage apoptosis and polarization via the JAK-STAT pathway in mice. Cell death & disease. 2024. doi:10.1038/s41419-024-06756-w. PMID: 38849370.
BibTeX
@article{cui2024-38849370,
author = {Cui, Y. and Chen, C. and Tang, Z. and Yuan, W. and Yue, K. and Cui, P. and Qiu, X. and Zhang, H. and others},
title = {{TREM2 deficiency aggravates renal injury by promoting macrophage apoptosis and polarization via the JAK-STAT pathway in mice}},
journal = {Cell death \& disease},
year = {2024},
doi = {10.1038/s41419-024-06756-w},
pmid = {38849370},
url = {https://doi.org/10.1038/s41419-024-06756-w}
}
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
- Its role in renal injury, in particular, unilateral ureteral obstruction (UUO) or ischemia-reperfusion injury (IRI)-induced renal injury remains unclear.
- In our study, WT and Trem2 -/- mice were employed to evaluate the role of TREM2 in renal macrophage infiltration and tissue injury after UUO.
- Bone marrow-derived macrophages (BMDM) from both mouse genotypes were cultured and polarized for in vitro experiments.
- Next, the effects of TREM2 on renal injury and macrophage polarization in IRI mice were also explored.
Why it matters
This study is about kidney injury, not Alzheimer's disease, and found that TREM2 deficiency worsened renal injury in mice by promoting macrophage apoptosis and polarization. It reports no Alzheimer's treatment, cure or prevention.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 47/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Cell death & disease) |
| Journal's citation record | 2 / 4 | Cell Death and Disease: journal h-index 233 (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 | 4 / 5 | 2024 — within 3 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 | Laboratory or animal study (title names “mice”) — scores zero |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 62 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.5 citations a year over 4 year(s) since 2024 |
| Impact for its field and year | 4 / 6 | Cited 8.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 3 / 4 | Cited 62 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Helong Dai: h-index 16 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Pittsburgh: institution h-index 1,470 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 38849370) |
| Free to read | 2 / 2 | Free to read |
| Total | 47 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1038/s41419-024-06756-w
- PubMed: 38849370
- Original source →
- Free full text: Cell Death and Disease →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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