ArticleMolecular metabolism2025
Epigenetic suppression of creatine kinase B in adipocytes links endoplasmic reticulum stress to obesity-associated inflammation.
Article in Molecular metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Paediatric proteomic signatures of cardiometabolic disease-associated traits predict adult disease outcomes.Nature metabolism · 2026Article
- Perspectives on human adipose tissue: from cellular mechanisms to clinical complications.Diabetologia · 2026Review
- Metabolism and homeostasis of energy in trophoblast cells of the placenta: from development to disease†.Biology of reproduction · 2026Review
- Complement System-Related Genes in Diabetic Nephropathy: Screening for Potential Targets of the Mechanism.Journal of diabetes research · 2026Article
- How Adipocytes Orchestrate Inflammation Within Adipose Tissue?Biomolecules · 2025Review
- Creation of Genetically Modified Adipocytes for Tissue Engineering: Creatine Kinase B Overexpression Leads to Stimulated Glucose Uptake and Mitochondrial Potential Growth, but Lowered Lipid Synthesis.Life (Basel, Switzerland) · 2025Article
- Car@PLGA-NPs target gut microbiota-ER stress axis to combat diabetes.Frontiers in cellular and infection microbiology · 2025Article
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Authors and funding
15 authors.
Funding
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Abstract
In white adipose tissue, disturbed creatine metabolism through reduced creatine kinase B (CKB) transcription contributes to obesity-related inflammation. However, the mechanisms regulating CKB expression in human white adipocytes remain unclear. By screening conditions perturbed in obesity, we identified endoplasmic reticulum (ER) stress as a key suppressor of CKB transcription across multiple cell types. Through follow-up studies, we found that ER stress through the IRE1-XBP1s pathway, promotes CKB promoter methylation via the methyltransferase DNMT3A. This epigenetic change represses CKB transcription, shifting metabolism towards glycolysis and increasing the production of the pro-inflammatory chemokine CCL2. We validated our findings in vivo, demonstrating that individuals living with obesity show an inverse relationship between CKB expression and promoter methylation in white adipocytes, along with elevated CCL2 secretion. Overall, our study uncovers a regulatory axis where ER stress drives inflammation in obesity by reducing CKB abundance, and consequently altering the bioenergetic state of the cell.
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