ArticleCell death & disease2022
B-cell lymphoma 6 alleviates nonalcoholic fatty liver disease in mice through suppression of fatty acid transporter CD36.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Hypothalamic BCL6 signaling modulates energy homeostasis and metabolism by inhibiting STAT3 transcription.Journal of advanced research · 2026Article
- A CD36-targeted aptamer-4-butyl-polyhydroxybenzophenone conjugate with pH-responsive release for liver delivery in MASLD.Regenerative biomaterials · 2026Article
- Article
- Chrysanthemum morifolium extract improves metabolic dysfunction-associated fatty liver disease by regulating lipid metabolism.Scientific reports · 2025Article
- Regulation of partial endothelial-to-mesenchymal transition by circATXN1 in ischemic diseases.Nature communications · 2025Article
- The effect of aldafermin expressing-Escherichia coli Nissle 1917 along with dietary change on visceral adipose tissue in MASLD mouse model.International journal of obesity (2005) · 2025Article
- BCL6 coordinates muscle mass homeostasis with nutritional states.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Ethyl Acetate Extract ofMetabolites · 2025Article
- MOR23 deficiency exacerbates hepatic steatosis in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Chemically synthesized osteocalcin alleviates NAFLD via the AMPK-FOXO1/BCL6-CD36 pathway.Journal of translational medicine · 2024Article
- The Different Mechanisms of Lipid Accumulation in Hepatocytes Induced by Oleic Acid/Palmitic Acid and High-Fat Diet.Molecules (Basel, Switzerland) · 2023Article
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- Myeloid-CITED2 Deficiency Exacerbates Diet-Induced Obesity and Pro-Inflammatory Macrophage Response.Cells · 2023Article
- Traditional Chinese medicines and natural products targeting immune cells in the treatment of metabolic-related fatty liver disease.Frontiers in pharmacology · 2023Review
- Deletion ofProceedings of the National Academy of Sciences of the United States of America · 2022Article
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Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD) is an ubiquitous disease that exists across a wide spectrum ranging from steatosis, steatohepatitis, advanced fibrosis, and liver cirrhosis. Hallmarks of NAFLD are lipid accumulation, insulin resistance, and chronic low-grade inflammation. However, there currently are no medications approved for NAFLD. B-cell lymphoma 6 (BCL6) is a transcriptional inhibitor that is vital for germinal center B-cell formation. Our study identified BCL6 as a critical modulator of hepatic lipid metabolism and appears to contribute to the initiation and progression of NAFLD. In our research, we induced hepatic BCL6 overexpression using adeno-associated virus (AAV), as well as conditional liver-specific BCL6 knockout mice (BCL6-CKO). With these models, we noted that BCL6 overexpression improved insulin resistance and hepatic steatosis in mice models maintained on a HFD diet. Conversely, these parameters worsened in the livers of mice with downregulated BCL6 levels. Mechanistically, the translocase fatty acid CD36 was determined to be a transcriptional target of BCL6 that influences its role in hepatic steatosis. BCL6 bound directly to the CD36 promoter region, restraining CD36 transcription under physiological conditions. We conclude that the hepatocyte BCL6 inhibits the NAFLD progression in mice, including deranged lipid accumulation and glucose metabolism, through a CD36-dependent manner. These results indicate that BCL6 may potentially be targeted in NAFLD treatment.
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