The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Mitochondrial dysfunction in macrophages promotes inflammation and suppresses repair after myocardial infarction
Open accessAbstract
Innate immune cells play important roles in tissue injury and repair following acute myocardial infarction (MI). Although reprogramming of macrophage metabolism has been observed during inflammation and resolution phases, the mechanistic link to macrophage phenotype is not fully understood. In this study, we found that myeloid-specific deletion (mKO) of mitochondrial complex I protein, encoded by Ndufs4, reproduced the proinflammatory metabolic profile in macrophages and exaggerated the response to LPS. Moreover, mKO mice showed increased mortality, poor scar formation, and worsened cardiac function 30 days after MI. We observed a greater inflammatory response in mKO mice on day 1 followed by increased cell death of infiltrating macrophages and blunted transition to the reparative phase during post-MI days 3-7. Efferocytosis was impaired in mKO macrophages, leading to lower expression of antiinflammatory cytokines and tissue repair factors, which suppressed the proliferation and activation of myofibroblasts in the infarcted area. Mitochondria-targeted ROS scavenging rescued these impairments, improved myofibroblast function in vivo, and reduced post-MI mortality in mKO mice. Together these results reveal a critical role of mitochondria in inflammation resolution and tissue repair via modulation of efferocytosis and crosstalk with fibroblasts. These findings have potential significance for post-MI recovery as well as for other inflammatory conditions.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
MANTOVANI, A., SOZZANI, S., LOCATI, M., ALLAVENA, P., & SICA, A. (2002) · Trends in Immunology · doi:10.1016/s1471-4906(02)02302-5 · Cited by 5,528
Mills, E. L., Kelly, B., Logan, A., Costa, A. S. H., Varma, M., Bryant, C. E., Tourlomousis, P., Däbritz, J. H. M., Gottlieb, E., Latorre, I., et al. (2016) · Cell · doi:10.1016/j.cell.2016.08.064 · Cited by 2,291
Conditional gene targeting in macrophages and granulocytes using LysMcre mice
Clausen, B. E., Burkhardt, C., Reith, W., Renkawitz, R., & Förster, I. (1999) · Transgenic Research · doi:10.1023/a:1008942828960 · Cited by 2,098
The inflammatory response in myocardial injury, repair, and remodelling
Frangogiannis, N. G. (2014) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2014.28 · Cited by 1,738
Tlr signalling augments macrophage bactericidal activity through mitochondrial ros
West, A. P., Brodsky, I. E., Rahner, C., Woo, D. K., Erdjument-Bromage, H., Tempst, P., Walsh, M. C., Choi, Y., Shadel, G. S., & Ghosh, S. (2011) · Nature · doi:10.1038/nature09973 · Cited by 1,659
Regulation of the Inflammatory Response in Cardiac Repair
Frangogiannis, N. G. (2012) · Circulation Research · doi:10.1161/circresaha.111.243162 · Cited by 1,194
Rodríguez-Prados, J.-C., Través, P. G., Cuenca, J., Rico, D., Aragonés, J., Martín-Sanz, P., Cascante, M., & Boscá, L. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.0901698 · Cited by 1,022
Bone Marrow-Derived Macrophages (BMM): Isolation and Applications
Weischenfeldt, J., & Porse, B. (2008) · Cold Spring Harbor Protocols · doi:10.1101/pdb.prot5080 · Cited by 955
A Novel and Efficient Model of Coronary Artery Ligation and Myocardial Infarction in the Mouse
Gao, E., Lei, Y. H., Shang, X., Huang, Z. M., Zuo, L., Boucher, M., Fan, Q., Chuprun, J. K., Ma, X. L., & Koch, W. J. (2010) · Circulation Research · doi:10.1161/circresaha.110.223925 · Cited by 760
Myocardial remodeling after infarction: the role of myofibroblasts
van den Borne, S. W. M., Diez, J., Blankesteijn, W. M., Verjans, J., Hofstra, L., & Narula, J. (2010) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2009.199 · Cited by 739
Cited by
Tissue macrophages: origin, heterogenity, biological functions, diseases and therapeutic targets
Guan, F., Wang, R., Yi, Z., Luo, P., Liu, W., Xie, Y., Liu, Z., Xia, Z., Zhang, H., & Cheng, Q. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02124-y · Cited by 371
Wang, S., Pei, G., Shen, J., Fang, Z., Chen, T., Wang, L., Cheng, H., Li, H., Pei, H., Feng, Q., et al. (2026) · Journal of Advanced Research · doi:10.1016/j.jare.2025.04.019 · Cited by 6
“Inflammation is a key process after MI and is characterized by extensive cell death and inflammatory cell infiltration [34,35].”
Metadata
- Authors
- Cai, S., Zhao, M., Zhou, B., Yoshii, A., Bugg, D., Villet, O., Sahu, A., Olson, G. S., Davis, J., & Tian, R.
- Venue
- Journal of Clinical Investigation
- Published
- 2023-02-15
- Volume
- 133
- Issue
- 4
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- OpenAlex
- W4310963001
- Cited by
- 282
- References
- 44
- FWCI
- 33.89
- Type
- journal article
- Language
- en
- Open access
- gold
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Mitochondrial dysfunction in macrophages promotes inflammation and suppresses repair after myocardial infarction. https://app.cochat.ai/papers/10.1172/jci159498
- The paper
- Cai, S., Zhao, M., Zhou, B., Yoshii, A., Bugg, D., Villet, O., Sahu, A., Olson, G. S., Davis, J., & Tian, R. (2023). Mitochondrial dysfunction in macrophages promotes inflammation and suppresses repair after myocardial infarction. Journal of Clinical Investigation. https://doi.org/10.1172/jci159498
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
