Home › Research › TREM2 and immune genetics
TREM2 macrophage promotes cardiac repair in myocardial infarction by reprogramming metabolism via SLC25A53
Gong S, Zhai M, Shi J, Yu G, Lei Z, Shi Y, Zeng Y, Ju P et al.. Cell death and differentiation, 2024-01-05
Topic: Brain proteins, microglia and lab models
Efferocytosis and metabolic reprogramming of macrophages play crucial roles in myocardial infarction (MI) repair. TREM2 has been proven to participate in phagocytosis and metabolism, but how it modulates myocardial infarction remains unclear. In this study, we showed that macrophage-specific TREM2 deficiency worsened cardiac function and impaired post-MI repair.
Key findings
- TREM2 has been proven to participate in phagocytosis and metabolism, but how it modulates myocardial infarction remains unclear.
- In this study, we showed that macrophage-specific TREM2 deficiency worsened cardiac function and impaired post-MI repair.
- Using RNA-seq, protein and molecular docking, and Targeted Metabolomics (LC-MS), our data demonstrated that macrophages expressing TREM2 exhibited decreased SLC25A53 transcription through the SYK-SMAD4 signaling pathway after efferocytosis, which impaired NAD + transport into mitochondria, downregulated SLC25A53 thereby causing the breakpoint in the TCA cycle and subsequently increased itaconate production.
- In vitro experiments confirmed that itaconate secreted by TREM2 + macrophages inhibited cardiomyocyte apoptosis and promoted fibroblast proliferation.
Why it matters
This study is about heart attack repair, not Alzheimer's disease, and shows that macrophage TREM2 deficiency worsens cardiac function after myocardial infarction. It provides no information on treating, curing or preventing Alzheimer's disease.
New to this subject? Start with our plain-English guide: Genetics →
Study details
- Evidence strengthLow
How this study scored 51/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Cell death and differentiation) |
| Journal's citation record | 3 / 4 | Cell Death and Differentiation: journal h-index 313 (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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 117 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 29.2 citations a year over 4 year(s) since 2024 |
| Impact for its field and year | 5 / 6 | Cited 31.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 3 / 4 | Cited 117 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Wenhui Peng: h-index 28 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Shanghai Jiao Tong University: institution h-index 975 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 9 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 38182899) |
| Free to read | 2 / 2 | Free to read |
| Total | 51 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1038/s41418-023-01252-8
- PubMed: 38182899
- Original source →
- Free full text: Cell Death and Differentiation →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
Gong, S., Zhai, M., Shi, J., Yu, G., Lei, Z., Shi, Y., et al. (2024). TREM2 macrophage promotes cardiac repair in myocardial infarction by reprogramming metabolism via SLC25A53. Cell death and differentiation. https://doi.org/10.1038/s41418-023-01252-8
Vancouver
Gong S, Zhai M, Shi J, Yu G, Lei Z, Shi Y, et al. TREM2 macrophage promotes cardiac repair in myocardial infarction by reprogramming metabolism via SLC25A53. Cell death and differentiation. 2024. doi:10.1038/s41418-023-01252-8. PMID: 38182899.
BibTeX
@article{gong2024-38182899,
author = {Gong, S. and Zhai, M. and Shi, J. and Yu, G. and Lei, Z. and Shi, Y. and Zeng, Y. and Ju, P. and others},
title = {{TREM2 macrophage promotes cardiac repair in myocardial infarction by reprogramming metabolism via SLC25A53}},
journal = {Cell death and differentiation},
year = {2024},
doi = {10.1038/s41418-023-01252-8},
pmid = {38182899},
url = {https://doi.org/10.1038/s41418-023-01252-8}
}
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.
Related studies in TREM2 and immune genetics
Also tagged “macrophages”
363 studies in the library carry the topic tag “macrophages”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 363 tagged studies.