ArticleMammalian genome : official journal of the International Mammalian Genome Society2024
E3 ubiquitin ligase COP1-mediated CEBPB ubiquitination regulates the inflammatory response of macrophages in sepsis-induced myocardial injury.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- O‑GlcNAcylation: The crosstalk between infection immunity and autophagy in sepsis (Review).Molecular medicine reports · 2025Review
- COP1 Overexpression Attenuates Nociceptive Behaviors and Neuroinflammation in Cancer-Induced Bone Pain by Suppressing c/EBPβ.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Pathological roles of ubiquitination and deubiquitination systems in sepsis-induced myocardial dysfunction.Biomolecules & biomedicine · 2025Review
- Bulk and Single-Cell Transcriptomic Reveals Shared Key Genes and Patterns of Immune Dysregulation in Both Intestinal Inflammatory Disease and Sepsis.Journal of cellular and molecular medicine · 2025Article
- The Ubiquitin-Proteasome System: A Key Regulatory Hub in Myocarditis Leading to Dilated Cardiomyopathy.Journal of inflammation research · 2025Review
- Post-translational modifications in sepsis-induced organ dysfunction: mechanisms and implications.Frontiers in immunology · 2024Review
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
CCAAT/enhancer-binding protein beta (CEBPB) has been associated with sepsis. However, its role in sepsis-induced myocardial injury (SIMI) remains ill-defined. This research was designed to illustrate the involvement of CEBPB in SIMI and its upstream modifier. The transcriptomic changes in heart biopsies of mice that had undergone polymicrobial sepsis were downloaded from the GEO dataset for KEGG enrichment analysis. CEBPB, on the TNF signaling pathway, was significantly enhanced in the myocardial tissues of mice with SIMI. Downregulation of CEBPB alleviated SIMI, as evidenced by minor myocardial injury and inflammatory manifestations. Moreover, ubiquitination modification of CEBPB by constitutive photomorphogenesis protein 1 homolog (COP1) led to the degradation of CEBPB and inhibited inflammatory responses in macrophages. Upregulation of COP1 protected against SIMI in mice overexpressing CEBPB. Collectively, our findings demonstrated that COP1 protected the heart against SIMI through the ubiquitination modification of CEBPB, which might be a novel therapeutic approach in the future.
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