The liver is one of the few organs that retain the capability to regenerate in adult mammals. This regeneration process is mainly facilitated by the dynamic behavior of hepatocytes, which are the major functional constituents in the liver. In response to liver injury, hepatocytes undergo remarkable alterations, such as reprogramming, wherein they lose their original identity and acquire properties from other cells. This phenomenon of hepatocyte reprogramming, coupled with hepatocyte expansion, plays a central role in liver regeneration, and its underlying mechanisms are complex and multifaceted. Understanding the fate of reprogrammed hepatocytes and the mechanisms of their conversion has significant implications for the development of innovative therapeutics for liver diseases. Herein, we review the plasticity of hepatocytes in response to various forms of liver injury, with a focus on injury-induced hepatocyte reprogramming. We provide a comprehensive summary of current knowledge on the molecular and cellular mechanisms governing hepatocyte reprogramming, specifically in the context of liver regeneration, providing insight into potential applications of this process in the treatment of liver disorders, including chronic liver diseases and liver cancer.
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http://dx.doi.org/10.1111/febs.16930 | DOI Listing |
Adv Sci (Weinh)
January 2025
Fujian Key Laboratory of Coastal Pollution Prevention and Control, Xiamen University, Xiamen, 361102, China.
Bisphenol A (BPA) is an "environmental obesogen" and this study aims to investigate the intergenerational impacts of BPA-induced metabolic syndrome (MetS), specifically focusing on unraveling mechanisms. Exposure to BPA induces metabolic disorders in the paternal mice, which are then transmitted to offspring, leading to late-onset MetS. Mechanistically, BPA upregulates Srebf1, which in turn promotes the Pparg-dependent transcription of Dicer1 in spermatocytes, increasing the levels of multiple sperm microRNAs (miRNAs).
View Article and Find Full Text PDFAnimal Model Exp Med
December 2024
GemPharmatech Chengdu Co., Ltd., Chengdu, China.
Background: The emerging incidence of pathogenic liver conditions is turning into a major concern for global health. Induction of pyroptosis in hepatocytes instigates cellular disintegration, which in turn liberates substantial quantities of pro-inflammatory intracellular substances, thereby accelerating the advancement of liver fibrosis. Consequently, directing therapeutic efforts towards inhibiting pyroptosis could potentially serve as an innovative approach in managing inflammation related chronic hepatic disorders.
View Article and Find Full Text PDFPharmacol Res
January 2025
State Key Laboratory of Natural Medicines and Jiangsu Key Laboratory of Bioactive Natural Product Research, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 210009, China. Electronic address:
Limb expression 1-like protein (LIX1L) is an essential player in liver disorders, but its function in metabolic dysfunction-associated steatohepatitis (MASH) and associated hepatocellular carcinoma (HCC) progression remains obscure. Here, we identify LIX1L as a key integrative regulator linking lipid metabolism and inflammation, adipose tissue and hepatic microenvironment, which promotes MASH progression. LIX1L significantly upregulates in MASH patients, mouse models, and palmitic acid-stimulated hepatocytes.
View Article and Find Full Text PDFbioRxiv
December 2024
Division of Molecular Medicine, Department of Medicine, University of Minnesota, Minneapolis, MN USA.
Metabolic reprogramming is a hallmark of cancer, enabling tumor cells to adapt to and exploit their microenvironment for sustained growth. The liver is a common site of metastasis, but the interactions between tumor cells and hepatocytes remain poorly understood. In the context of liver metastasis, these interactions play a crucial role in promoting tumor survival and progression.
View Article and Find Full Text PDFFront Immunol
December 2024
Department of Biochemistry, Faculty of Medicine, Medical University of Warsaw, Warsaw, Poland.
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