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HMOX1-LDHB interaction promotes ferroptosis by inducing mitochondrial dysfunction in foamy macrophages during advanced atherosclerosis
Peng X, Sun B, Tang C, Shi C, Xie X, Wang X, Jiang D, Li S et al.. Developmental cell, 2024-12-27
Topic: Brain proteins, microglia and lab models
Advanced atherosclerosis is the pathological basis for acute cardiovascular events, with significant residual risk of recurrent clinical events despite contemporary treatment. The death of foamy macrophages is a main contributor to plaque progression, but the underlying mechanisms remain unclear. Bulk and single-cell RNA sequencing demonstrated that massive iron accumulation in advanced atherosclerosis promoted foamy macrophage ferroptosis, particularly in low expression of triggering receptor expressed on myeloid cells 2 (TREM2 low ) foamy macrophages.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Peng, X., Sun, B., Tang, C., Shi, C., Xie, X., Wang, X., et al. (2025). HMOX1-LDHB interaction promotes ferroptosis by inducing mitochondrial dysfunction in foamy macrophages during advanced atherosclerosis. Developmental cell. https://doi.org/10.1016/j.devcel.2024.12.011
Vancouver
Peng X, Sun B, Tang C, Shi C, Xie X, Wang X, et al. HMOX1-LDHB interaction promotes ferroptosis by inducing mitochondrial dysfunction in foamy macrophages during advanced atherosclerosis. Developmental cell. 2025. doi:10.1016/j.devcel.2024.12.011. PMID: 39731912.
BibTeX
@article{peng2025-39731912,
author = {Peng, X. and Sun, B. and Tang, C. and Shi, C. and Xie, X. and Wang, X. and Jiang, D. and Li, S. and others},
title = {{HMOX1-LDHB interaction promotes ferroptosis by inducing mitochondrial dysfunction in foamy macrophages during advanced atherosclerosis}},
journal = {Developmental cell},
year = {2025},
doi = {10.1016/j.devcel.2024.12.011},
pmid = {39731912},
url = {https://doi.org/10.1016/j.devcel.2024.12.011}
}
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Key findings
- The death of foamy macrophages is a main contributor to plaque progression, but the underlying mechanisms remain unclear.
- Bulk and single-cell RNA sequencing demonstrated that massive iron accumulation in advanced atherosclerosis promoted foamy macrophage ferroptosis, particularly in low expression of triggering receptor expressed on myeloid cells 2 (TREM2 low ) foamy macrophages.
- This cluster exhibits metabolic characteristics with low oxidative phosphorylation (OXPHOS), increasing ferroptosis sensitivity.
- Mechanically, upregulated heme oxygenase 1 (HMOX1)-lactate dehydrogenase B (LDHB) interaction enables Lon peptidase 1 (LONP1) to degrade mitochondrial transcription factor A (TFAM), leading to mitochondrial dysfunction and ferroptosis.
Why it matters
This study found that iron accumulation promoted ferroptosis of foamy macrophages in advanced atherosclerosis, particularly in TREM2-low cells. It is about atherosclerosis and not Alzheimer's disease, so it has no implications for treating, curing or preventing Alzheimer's.
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Study details
- Evidence strengthLow
How this study scored 49/100
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 (Developmental cell) |
| Journal's citation record | 3 / 4 | Developmental Cell: journal h-index 359 (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 | 2025 — 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 | 4 / 7 | Cited 64 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 21.3 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 4 / 6 | Cited 16.5× 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 64 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Jinwei Tian: h-index 33 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Chinese Academy of Medical Sciences & Peking Union Medical College: institution h-index 950 (OpenAlex) |
| Multi-centre collaboration | 3 / 3 | OpenAlex lists 15 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39731912) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 49 / 100 | — |
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