ArticleThe Journal of clinical investigation2024
Hepatocyte-specific CCAAT/enhancer binding protein α restricts liver fibrosis progression.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 22 citations in OpenAlex.
- siRNA therapeutics for metabolic dysfunction-associated Steatohepatitis: Targets, delivery, clinical evidence, and translational challenges.Biochemistry and biophysics reports · 2026Review
- Review
- P-STAT3-dependent SPP1 transcription in cholangiocytes drives hepatic stellate cells activation in congenital hepatic fibrosis.Communications biology · 2026Article
- Resveratrol Alleviates Arsenic-Induced Liver Fibrosis in Rats by Correcting SIRT1-Mediated Disorder of Hepatic Bile Acid Metabolism.International journal of molecular sciences · 2026Article
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- An LSEC-focused computational drug repurposing platform for liver fibrosis: Identification of vorinostat and other LSEC-protective candidates.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms and reversal strategies of liver fibrosis: from regulation of cell fate to clinical translation.Journal of translational medicine · 2026Review
- Glyphosate-Induced Metabolic and Immune Modulation in Hepatoma Cells: Identification of Key Genes as Diagnostic and Therapeutic Targets Using an In Silico Systems Biology Approach.Journal of xenobiotics · 2026Article
- Targeting CEBPA/ALOX15B attenuates postmenopausal osteoporosis by inhibiting ferroptosis through the AMPK/mTOR signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- A novel C/EBPα-miR-335-5p-PRKAA2 regulatory axis drives hepatic lipid accumulation in MASLD.Scientific reports · 2026Article
- Gut Microbiota-Derived Propionic Acid Mediates ApoA-I-Induced Amelioration of MASLD via Activation of GPR43-CaInternational journal of molecular sciences · 2026Article
- Epithelial membrane protein 1 drives hepatic stellate cell activation via the TLN1/FAK cascade in MASLD donor liver transplantation.Molecular biomedicine · 2025Article
- The GLP-1 Receptor Agonist Dulaglutide Attenuates Hepatic Steatosis in Obesity via a Weight-Independent Mechanism.Diabetes · 2025Article
- The Non-Canonical ChREBPα Activity Suppresses the Activation of Hepatic Stellate Cells and Liver Fibrosis by Antagonizing TGF-β-E2F1 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single cell multiomics reveals drivers of metabolic dysfunction-associated steatohepatitis.medRxiv : the preprint server for health sciences · 2025Article
- Tumor cell-derived osteopontin promotes tumor fibrosis indirectly via tumor-associated macrophages.Journal of translational medicine · 2025Article
- Research Progress on the Role and Mechanism of Flavonoids in Improving Metabolic Associated Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- The immune duality of osteopontin and its therapeutic implications for kidney transplantation.Frontiers in immunology · 2025Review
- Non-coding RNAs: emerging biomarkers and therapeutic targets in cancer and inflammatory diseases.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 3 countries.
Funding
Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) - previously described as nonalcoholic steatohepatitis (NASH) - is a major driver of liver fibrosis in humans, while liver fibrosis is a key determinant of all-cause mortality in liver disease independent of MASH occurrence. CCAAT/enhancer binding protein α (CEBPA), as a versatile ligand-independent transcriptional factor, has an important function in myeloid cells, and is under clinical evaluation for cancer therapy. CEBPA is also expressed in hepatocytes and regulates glucolipid homeostasis; however, the role of hepatocyte-specific CEBPA in modulating liver fibrosis progression is largely unknown. Here, hepatic CEBPA expression was found to be decreased during MASH progression both in humans and mice, and hepatic CEBPA mRNA was negatively correlated with MASH fibrosis in the human liver. CebpaΔHep mice had markedly enhanced liver fibrosis induced by a high-fat, high-cholesterol, high-fructose diet or carbon tetrachloride. Temporal and spatial hepatocyte-specific CEBPA loss at the progressive stage of MASH in CebpaΔHep,ERT2 mice functionally promoted liver fibrosis. Mechanistically, hepatocyte CEBPA directly repressed Spp1 transactivation to reduce the secretion of osteopontin, a fibrogenesis inducer of hepatic stellate cells. Forced hepatocyte-specific CEBPA expression reduced MASH-associated liver fibrosis. These results demonstrate an important role for hepatocyte-specific CEBPA in liver fibrosis progression, and may help guide the therapeutic discoveries targeting hepatocyte CEBPA for the treatment of liver fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.