ArticleInternational journal of biological sciences2015
A20 Attenuates FFAs-induced Lipid Accumulation in Nonalcoholic Steatohepatitis.
Article in International journal of biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- The emerging role of E3 ubiquitin ligases and deubiquitinases in metabolic dysfunction-associated steatotic liver disease.Journal of translational medicine · 2025Review
- Epidermal growth factor upregulates the expression of A20 in hepatic cells via the MEK1/MSK1/p-p65 (Ser276) signaling pathway.American journal of translational research · 2021Article
- LRRK2 Regulates CPT1A to Promote β-Oxidation in HepG2 Cells.Molecules (Basel, Switzerland) · 2020Article
- Combined All-Extremity High-Intensity Interval Training Regulates Immunometabolic Responses through Toll-Like Receptor 4 Adaptors and A20 Downregulation in Obese Young Females.Obesity facts · 2020Article
- Allantoin improves methionine-choline deficient diet-induced nonalcoholic steatohepatitis in mice through involvement in endoplasmic reticulum stress and hepatocytes apoptosis-related genes expressions.Iranian journal of basic medical sciences · 2019Article
- The deubiquitinating enzyme TNFAIP3 mediates inactivation of hepatic ASK1 and ameliorates nonalcoholic steatohepatitis.Nature medicine · 2018Article
- Elevated serum A20 is associated with severity of chronic hepatitis B and A20 inhibits NF-κB-mediated inflammatory response.Oncotarget · 2017Article
- A20 Attenuates Liver Fibrosis in NAFLD and Inhibits Inflammation Responses.Inflammation · 2017Article
- An ErChen and YinChen Decoction Ameliorates High-Fat-Induced Nonalcoholic Steatohepatitis in Rats by Regulating JNK1 Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- A20 reduces lipid storage and inflammation in hypertrophic adipocytes via p38 and Akt signaling.Molecular and cellular biochemistry · 2016Article
- The effect of polyene phosphatidyl choline intervention on nonalcoholic steatohepatitis and related mechanism.American journal of translational research · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A20 is a ubiquitin-editing enzyme that attenuates the activity of proximal signaling complexes at pro-inflammatory receptors. It has been well documented that A20 protein plays an important role in response to liver injury and hepatocytes apoptosis in pro-inflammatory pathways. However, there was little evidence showing that A20 protein was involving in fatty-acid homeostasis except the up-regulation of two fatty acid metabolism regulatory genes at mRNA level (PPARa and CPT1a) by adenovirus-mediated A20 protein overexpression. In this study we found that: 1) the expression level of A20 protein was significantly higher in the steatotic liver from MCD-fed mice than the controls; 2) Overexpression of A20 protein suppressed FFAs-stimulated triglyceride deposition in HepG2 cells while under expression of A20 protein increased FFAs-stimulated triglyceride deposition; 3) Overexpression of A20 protein in HepG2 cells upregulated genes that promote β-oxidation and decreased the mRNA levels of key lipogenic genes such as fatty acid synthase (FAS), indicating A20 function as anti-steatotic factor by the activation of mitochondrial β-oxidation and attenuation of de novo lipogenesis; 4) Nonalcoholic steatohepatitis (NASH) patients showed significantly higher A20 expression level in liver compared with control individuals. Our results demonstrated that A20 protein plays an important role in fatty-acid homeostasis in human as well as animals. In addition, our data suggested that the pathological function of A20 protein in hepatocyte from lipotoxicity to NASH is by the alleviation of triglyceride accumulation in hepatocytes. Elevated expression of A20 protein could be a potential therapeutic strategy for preventing the progression of nonalcoholic steatohepatitis.
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