Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3437919 | PMC |
| http://dx.doi.org/10.1021/cr2001355 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Effects of combined stressors to TCDD and high temperature on HSP/CYPs signaling in the zebrafish embryos/larvae.
Environ Pollut
March 2025
College of Animal Science and Technology, Inner Mongolia Minzu University, Tongliao, Inner Mongolia, 028000, China; Inner Mongolia Key Laboratory of Toxicant Monitoring and Toxicology. Electronic address:
Global warming causes the release of dioxin-like deposits and increases geographical migration, increasing the risk of exposure for humans and animals. In this experiment, we used CYP1A transgenic zebrafish Tg (cyp1a: mCherry) and liver fluorescent transgenic zebrafish Tg (fabp10: Ps Red) as an animal model and exposed to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD) at 26 °C and 30 °C, respectively. Morphological changes, histological changes, transcriptome and related genes expression were detected.
View Article and Find Full Text PDFCRSP8-driven fatty acid metabolism reprogramming enhances hepatocellular carcinoma progression by inhibiting RAN-mediated PPARα nucleus-cytoplasm shuttling.
J Exp Clin Cancer Res
March 2025
Department of Infectious Diseases, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510630, China.
Background: In-depth exploration into the dysregulation of lipid metabolism in hepatocellular carcinoma (HCC) has contributed to the development of advanced antitumor strategies. CRSP8 is a critical component of mediator multiprotein complex involved in transcriptional recruiting. However, the regulatory mechanisms of CRSP8 on fatty acid metabolism reprogramming and HCC progression remain unclear.
View Article and Find Full Text PDFFat-1 Ameliorates Metabolic Dysfunction-Associated Fatty Liver Disease and Atherosclerosis through Promoting the Nuclear Localization of PPARα in Hamsters.
Research (Wash D C)
March 2025
Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
Fat-1, an enzyme encoded by the gene, is responsible for the conversion of endogenous omega-6 polyunsaturated fatty acids into omega-3 polyunsaturated fatty acids in . To better investigate whether the expression of Fat-1 will exert a beneficial function in dyslipidemia and metabolic dysfunction-associated fatty liver disease (MAFLD), we established an adeno-associated virus 9 expressing Fat-1. We found that adeno-associated-virus-mediated expression of Fat-1 markedly reduced the levels of plasma triglycerides and total cholesterol but increased high-density lipoprotein levels in male wild-type hamsters on both chow diet and high-fat diet as well as in chow-diet-fed male LDLR hamsters.
View Article and Find Full Text PDFDeciphering PFAS Mode of Action: Comparative Gene Expression Analysis in Human Liver Spheroids.
Toxicol Sci
March 2025
Environmental Health Science and Research Bureau, Health Canada.
Understanding the mechanisms by which environmental chemicals cause toxicity is necessary for effective human health risk assessment. High-Throughput Transcriptomics (HTTr) can be used to inform risk assessment on toxicological mechanisms, hazards, and potencies. We applied HTTr to elucidate the molecular mechanisms by which Per- and Polyfluoroalkyl Substances (PFAS) cause liver perturbations.
View Article and Find Full Text PDFDifferential hepatic activation of mouse and human peroxisome proliferator-activated receptor-α by perfluorohexane sulfonate.
Toxicol Sci
February 2025
Department of Veterinary and Biomedical Science and Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania.
Exposure of perfluorohexane sulfonate (PFHxS) is associated with hepatomegaly and accumulation of lipids that may be mediated by nuclear receptors like peroxisome proliferator-activated receptor-α (PPARα), constitutive androstane receptor (CAR), or pregnane X receptor (PXR). This study tested the hypotheses that: 1) PFHxS causes changes in liver by activating PPARα, CAR or PXR, and 2) there is a species difference in PPARα activity by PFHxS. Wild-type, Ppara-null, and PPARA-humanized mice were fed either a control diet, or one containing 2.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!