The miR-23-27-24 clusters drive lipid-associated macrophage proliferation in obese adipose tissue
Open accessAbstract
Identifying molecular circuits that control adipose tissue macrophage (ATM) function is necessary to understand how ATMs contribute to tissue homeostasis and obesity-induced insulin resistance. In this study, we find that mice with a myeloid-specific knockout of the miR-23-27-24 clusters of microRNAs (miRNAs) gain less weight on a high-fat diet but exhibit worsened glucose and insulin tolerance. Analysis of ATMs from these mice shows selectively reduced numbers and proliferation of a recently reported subset of lipid-associated CD9 + Trem2 + ATMs (lipid-associated macrophages [LAMs]). Leveraging the role of miRNAs to control networks of genes, we use RNA sequencing (RNA-seq), functional screens, and biochemical assays to identify candidate target transcripts that regulate proliferation-associated signaling. We determine that miR-23 directly targets the mRNA of Eif4ebp2 , a gene that restricts protein synthesis and proliferation in macrophages. Altogether, our study demonstrates that control of proliferation of a protective subset of LAMs by noncoding RNAs contributes to protection against diet-induced obesity metabolic dysfunction.
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Overexpression of miR-23a-3p drives proliferation of lipid-associated macrophages in obese adipose tissue and prevents diet-induced obesity metabolic dysfunction.
“This also drives the proliferation of lipid-associated macrophages in obese adipose tissue and prevents diet-induced obesity metabolic dysfunction [21,22].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [22]
The Discussion (page not provided) says that myeloid expression of the miR-23–27-24 clusters supports lipid-associated macrophage proliferation and protects against obesity-induced metabolic dysfunction. The Results (page not provided) describe deletion of the clusters, not overexpression of miR-23a-3p alone, so the specific intervention attributed to this source is unsupported. (LLM, conf=0.86)
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Sekhon, H., Kageyama, R., Sprenkle, N. T., Happ, H. C., Wigton, E. J., Pua, H. H., & Ansel, K. M. (2025) · RNA Biology · doi:10.1080/15476286.2025.2564941
Self-citationADAR1 Controls Macrophage Scavenging and Lipid‐Buffering Programs in Metabolic Tissues
Fardellas, A., Barreby, E., Brice, M., Nock, S., Russick, J., Vankova, A., Edberg, C., Robertsen, I., Hertel, J. K., Stål, P., et al. (2026) · European Journal of Immunology · doi:10.1002/eji.70189 · Cited by 1 · see citing works
Wang, Z. D., Sun, M., Zhang, Z., Wang, Y., 佟胜杰, Meng, L., Han, D., Ge, X., Chen, H., Yang, D., et al. (2026) · Frontiers in Veterinary Science · doi:10.3389/fvets.2026.1794290
- Authors
- Sprenkle, N. T., Winn, N. C., Bunn, K. E., Zhao, Y., Park, D. J., Giese, B. G., Karijolich, J. J., Ansel, K. M., Serezani, C. H., Hasty, A. H., & Pua, H. H.
- Affiliations
- Vanderbilt University Medical Center (US)
- Vanderbilt University (US)
- University of California, San Francisco (US)
- Corresponding author
- Pua, Heather H.
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2023-08
- Volume
- 42
- Issue
- 8
- Pages
- 112928
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC10712211
- OpenAlex
- W4385521119
- Cited by
- 19
- References
- 71
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 5 · 2023: 2
- FWCI
- 3.79
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by-nc-nd)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Veterans Affairs (IK6BX005649)
- American Heart Association (21POST834990, 836819)
- Vanderbilt University (DK059637)
- Vanderbilt Institute for Clinical and Translational Research (UL1-TR002243)
- Vanderbilt University Medical Center (UL1 TR002243)
- National Institutes of Health (DK,059637, DK-020593, UL1TR002243)
- National Heart, Lung, and Blood Institute (R01HL109102)
- National Institute of General Medical Sciences (T32GM008554)
- National Institute of Allergy and Infectious Diseases (R21AI156292)
- National Institute of Diabetes and Digestive and Kidney Diseases (U24DK059637, P30DK020593)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- lipid-associated macrophages, adipose tissue macrophages, macrophage proliferation, obesity, insulin resistance, high-fat diet, myeloid-specific knockout, non-coding RNA, glucose tolerance, adipose tissue inflammation
- MeSH terms
- Adipose Tissue, Animals, Inflammation, Insulin Resistance, Lipids, Macrophages, Membrane Glycoproteins, Mice, Inbred C57BL, Obesity, Receptors, Immunologic, MicroRNAs, Cell Proliferation, Mice, Diet, High-Fat
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