ArticleJournal of molecular medicine (Berlin, Germany)2017
CREBH mediates metabolic inflammation to hepatic VLDL overproduction and hyperlipoproteinemia.
Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Elevated miR-34a induced by lipotoxicity and inflammation mediates pathophysiological communication between hepatocytes and hepatic stellate cells in liver fibrosis.Genes & diseases · 2025Article
- Hyperglycemia-induced overexpression of CREB3 L3 promotes the epithelial-to-mesenchymal transition in bladder urothelial cells in diabetes mellitus.World journal of diabetes · 2025Article
- Creb3l3 deficiency promotes intestinal lipid accumulation and alters ApoB-containing lipoprotein kinetics.Journal of lipid research · 2025Article
- Mechanistic role of long non-coding RNAs in the pathogenesis of metabolic dysfunction-associated steatotic liver disease and fibrosis.eGastroenterology · 2024Article
- Nonalcoholic fatty liver disease and insulin resistance in children.Clinical and experimental pediatrics · 2023Article
- Alterations of NMR-Based Lipoprotein Profile Distinguish Unstable Angina Patients with Different Severity of Coronary Lesions.Metabolites · 2023Article
- Palmitic acid induces intestinal lipid metabolism disorder, endoplasmic reticulum stress and inflammation by affecting phosphatidylethanolamine content in large yellow croakerFrontiers in immunology · 2022Article
- Schisantherin A alleviates non-alcoholic fatty liver disease by restoring intestinal barrier function.Frontiers in cellular and infection microbiology · 2022Article
- Endoplasmic Reticulum Stress Signaling and the Pathogenesis of Hepatocarcinoma.International journal of molecular sciences · 2021Review
- The Role of Mammalian Creb3-Like Transcription Factors in Response to Nutrients.Frontiers in genetics · 2019Review
- Non-parenchymal hepatic cell lipotoxicity and the coordinated progression of non-alcoholic fatty liver disease and atherosclerosis.Current opinion in lipidology · 2018Review
- CREBH Regulates Systemic Glucose and Lipid Metabolism.International journal of molecular sciences · 2018Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Metabolic inflammation is closely associated with hyperlipidemia and cardiovascular disease. However, the underlying mechanisms are not fully understood. The current study established that cAMP-responsive-element-binding protein H (CREBH), an acute-phase transcription factor, enhances very-low-density lipoprotein (VLDL) assembly and secretion by upregulating apolipoprotein B (apoB) expression and contributes to metabolic inflammation-associated hyperlipoproteinemia induced by TNFα, lipopolysaccharides (LPS), and high-fat diet (HFD) in mice. Specifically, overexpression of CREBH significantly induced mRNA and protein expression of apoB in McA-7777 cells. Luciferase assay further revealed that the presence of CREBH could significantly increase the activity of the apoB gene promoter. In contrast, genetic depletion of CREBH in mice resulted in significant reduction in expression of hepatic apoB mRNA. Challenging mice with an acute fat load led to upregulation of triglyceride (TG)-rich lipoprotein secretion in wild type mice, but not in CREBH-null mice. TNFα treatment activated hepatic CREBH expression, which in turn enhanced hepatic apoB biosynthesis and VLDL secretion. Metabolic inflammation induced by LPS or HFD also resulted in overproduction of apoB and hyperlipoproteinemia in wild type mice, but not in CREBH-null mice. This study demonstrates that CREBH could be a mediator between metabolic inflammation and hepatic VLDL overproduction in chronic metabolic disorders. This novel finding establishes CREBH as the first transcription factor that regulates apoB expression on the transcriptional level and the subsequent VLDL biosynthesis in response to metabolic inflammation. The study also provides novel insight into the pathogenesis of hyperlipidemia in metabolic syndrome. KEY MESSAGES: CREBH mediates inflammatory signaling to VLDL overproduction in metabolic stress. Activation of CREBH in inflammation enhances mRNA and protein expression of apoB. CREBH presents a potential novel therapeutic target for hyperlipoproteinemia.
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