ArticleCellular and molecular gastroenterology and hepatology2024
NCOA5 Haploinsufficiency in Myeloid-Lineage Cells Sufficiently Causes Nonalcoholic Steatohepatitis and Hepatocellular Carcinoma.
Article in Cellular and molecular gastroenterology and hepatology, 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, 8 citations in OpenAlex.
- The role of platelets in the hepatocellular carcinoma immune microenvironment and their clinical prospects: a comprehensive review.Medical oncology (Northwood, London, England) · 2026Review
- Applications of gene pair methods in clinical research: advancing precision medicine.Molecular biomedicine · 2025Review
- Immunotherapy resistance in MASLD-related hepatocellular carcinoma: special immune microenvironment and gut microbiota.International journal of biological sciences · 2025Review
- Macrophage-tregs crosstalk: the "hub" of the immune network in MASLD.Frontiers in immunology · 2025Review
- NCOA5 Deficiency in Macrophages Provokes NASH and HCC.Cellular and molecular gastroenterology and hepatology · 2024Article
- Prmt1-mediated histone H4R3me2a methylation regulates the proliferation, migration and invasion of laryngeal cancer cells by affecting the expression level of NCOA5.Frontiers in oncology · 2024Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsThe nuclear receptor coactivator 5 (NCOA5) is a putative type 2 diabetes susceptibility gene. NCOA5 haploinsufficiency results in the spontaneous development of nonalcoholic fatty liver disease (NAFLD), insulin resistance, and hepatocellular carcinoma (HCC) in male mice; however, the cell-specific effect of NCOA5 haploinsufficiency in various types of cells, including macrophages, on the development of NAFLD and HCC remains unknown.
methodsControl and myeloid-lineage-specific Ncoa5 deletion (Ncoa5
resultsMyeloid-lineage-specific Ncoa5 deletion sufficiently causes spontaneous NASH and HCC development in male mice fed a normal diet. PF4 overexpression in Ncoa5
conclusionsOur findings reveal a novel mechanism for the onset of NAFLD/NASH and HCC initiated by NCOA5-deficient macrophages, suggesting the NCOA5-PF4 axis in macrophages as a potential target for developing preventive and therapeutic interventions against NAFLD/NASH and HCC.
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