Nuclear factor Y participates in alcoholic liver disease by activating SREBP1 expression in mice

Zhang, Yanjie; Sun, Yajun; Zhang, Yange; Qin, Miao; Wang, Qi; Yang, Baohua; Li, Yanzhong; Li, Lin; Zhang, Ruiling

doi:10.1016/j.bbrc.2021.01.011

Cited by 3 publications

(2 citation statements)

References 29 publications

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“…Recently, NF-Y has been proven to participate in the early stages of alcoholic liver disease [ 69 ]; moreover, NF-Y, orchestrating the differential gene expression in response to acute alcohol intake, affects brain cell proliferation [ 70 ]. In particular, 6 h after ethanol (6 g/kg) administration in B6 and D2 mice, upregulation of NF-Y in the brain was determined by microarray analysis [ 70 ].…”

Section: Resultsmentioning

confidence: 99%

Reduction of Cell Proliferation by Acute C2H6O Exposure

Baldari¹,

Manni

Rocco

et al. 2021

Cancers

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Endogenous acetaldehyde production from the metabolism of ingested alcohol exposes hematopoietic progenitor cells to increased genotoxic risk. To develop possible therapeutic strategies to prevent or reverse alcohol abuse effects, it would be critical to determine the temporal progression of acute ethanol toxicity on progenitor cell numbers and proliferative status. We followed the variation of the cell proliferation rate in bone marrow and spleen in response to acute ethanol intoxication in the MITO-Luc mouse, in which NF-Y-dependent cell proliferation can be assessed in vivo by non-invasive bioluminescent imaging. One week after ethanol administration, bioluminescent signals in bone marrow and spleen decreased below the level corresponding to physiological proliferation, and they progressively resumed to pre-treatment values in approximately 4 weeks. Boosting acetaldehyde catabolism by administration of an aldehyde dehydrogenase activity activator or administration of polyphenols with antioxidant activity partially restored bone marrow cells’ physiological proliferation. These results indicate that in this mouse model, bioluminescent alteration reflects the reduction of the physiological proliferation rate of bone marrow progenitor cells due to the toxic effect of aldehydes generated by alcohol oxidation. In summary, this study presents a novel view of the impact of acute alcohol intake on bone marrow cell proliferation in vivo.

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Section: Resultsmentioning

confidence: 99%

Reduction of Cell Proliferation by Acute C2H6O Exposure

Baldari¹,

Manni

Rocco

et al. 2021

Cancers

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“…In addition, adiponectin-mediated FA oxidation via AMPK is reduced in chronic ethanol-fed rodent models (Xu et al, 2003;You et al, 2004). The nuclear factor Y (NF-Y) level was increased in the Gao-binge ethanol mice model, and NF-Y directly binds to the SREBP-1 promotor and increases its expression (Zhang et al, 2021). ethanol metabolism inhibit the function of pyruvate dehydrogenase and activate pyruvate carboxylase (Siess et al, 1978).…”

Section: Ethanol Alters Mitochondrial Metabolismmentioning

confidence: 99%

Insights of mitochondrial involvement in alcoholic fatty liver disease

Subramaiyam

2023

Journal Cellular Physiology

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Alcoholic liver disease (ALD) is a global concern affecting most of the population and leading to the development of end‐stage liver disease. Metabolic alterations due to increased alcohol consumption surge the hepatic accumulation of lipids and develop into a severe form of alcoholic steatohepatitis (ASH), depending on age and the consumption rate. The mitochondria in the hepatocyte actively regulate metabolic homeostasis and are disrupted in ALD pathogenesis. The increased NADH upon ethanol metabolism inhibits the mitochondrial oxidation of fatty acids, alters oxidative phosphorylation, and favors de novo lipogenesis. The higher mitochondrial respiration in early ALD increases free radical generation, whereas mitochondrial respiration is uncoupled in chronic ALD, affecting the cellular energy status. The defective glutathione importer due to excessive cholesterol loading and low adenosine triphosphate accounts for additional oxidative stress leading to hepatocyte apoptosis. The defective mitochondrial transcription machinery and sirtuins function in ALD affect mitochondrial function and biogenesis. The metabolites of ethanol metabolism epigenetically alter the gene expression profile of hepatic cell populations by modulating the promoters and sirtuins, aiding hepatic fibrosis and inflammation. The defect in mitophagy increases the accumulation of megamitochondria in hepatocytes and attracts immune cells by releasing mitochondrial damage‐associated molecular patterns to initiate hepatic inflammation and ASH progression. Thus, maintaining mitochondrial lipid homeostasis and antioxidant capacity pharmacologically could provide a better outcome for ALD management.

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The implications of FASN in immune cell biology and related diseases

Xiao,

Yang,

Xiong

et al. 2024

Cell Death Dis

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Fatty acid metabolism, particularly fatty acid synthesis, is a very important cellular physiological process in which nutrients are used for energy storage and biofilm synthesis. As a key enzyme in the fatty acid metabolism, fatty acid synthase (FASN) is receiving increasing attention. Although previous studies on FASN have mainly focused on various malignancies, many studies have recently reported that FASN regulates the survival, differentiation, and function of various immune cells, and subsequently participates in the occurrence and development of immune-related diseases. However, few studies to date systematically summarized the function and molecular mechanisms of FASN in immune cell biology and related diseases. In this review, we discuss the regulatory effect of FASN on immune cells, and the progress in research on the implications of FASN in immune-related diseases. Understanding the function of FASN in immune cell biology and related diseases can offer insights into novel treatment strategies for clinical diseases.

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Nuclear factor Y participates in alcoholic liver disease by activating SREBP1 expression in mice

Cited by 3 publications

References 29 publications

Reduction of Cell Proliferation by Acute C2H6O Exposure

Reduction of Cell Proliferation by Acute C2H6O Exposure

Insights of mitochondrial involvement in alcoholic fatty liver disease

The implications of FASN in immune cell biology and related diseases

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