ArticleBiochimica et biophysica acta. Molecular basis of disease2017
Growth arrest and DNA damage-inducible 45α protects against nonalcoholic steatohepatitis induced by methionine- and choline-deficient diet.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 61 citations in OpenAlex.
- The PERK-GADD45A axis is a key driver of hepatic stellate cell activation.Hepatology communications · 2026Article
- Single-Nucleotide Polymorphisms in Genes Associated with Mitochondrial and DNA Damage Response Modulate the Risk of Non-Alcoholic Fatty Liver Disease in Humans.International journal of molecular sciences · 2026Article
- GADD45β inhibits hepatic lipogenesis through the AMPK/SREBP1 pathway via reducing the ubiquitination-mediated degradation of SIRT1.Scientific reports · 2025Article
- GADD45A suppression contributes to cardiac remodeling by promoting inflammation, fibrosis and hypertrophy.Cellular and molecular life sciences : CMLS · 2025Article
- GADD45α is a direct target of TFEB and contributes to tacrolimus-induced chronic nephrotoxicity.JCI insight · 2025Article
- TRIB3 Is a Hub Gene in Steatohepatitis and Aggravates Lipid Deposition and Inflammation in Hepatocytes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Stress and Liver Fibrogenesis: Understanding the Role and Regulation of Stress Response Pathways in Hepatic Stellate Cells.The American journal of pathology · 2023Review
- High-fat diet in early life triggers both reversible and persistent epigenetic changes in the medaka fish (Oryzias latipes).BMC genomics · 2023Article
- Establishment of Novel Mouse Model of Dietary NASH Rapidly Progressing into Liver Cirrhosis and Tumors.Cancers · 2023Article
- Article
- Low Birth Weight Intensifies Changes in Markers of Hepatocarcinogenesis Induced by Fructose Consumption in Rats.Metabolites · 2022Article
- Gadd45 in Senescence.Advances in experimental medicine and biology · 2022Article
- The Interplay between Insulin Resistance, Inflammation, Oxidative Stress, Base Excision Repair and Metabolic Syndrome in Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2021Review
- GADD45A is a protective modifier of neurogenic skeletal muscle atrophy.JCI insight · 2021Article
- Article
- Antifibrotic Effects of Kangxian Ruangan Capsule on Rats with Nonalcoholic Fatty Liver Fibrosis and Hepatic Stellate Cells through Regulation of TGF-Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Histone H3K27 methyltransferase EZH2 and demethylase JMJD3 regulate hepatic stellate cells activation and liver fibrosis.Theranostics · 2021Article
- Comparative analysis of the expression profiles of genes related to the Gadd45α signaling pathway in four kinds of liver diseases.Histology and histopathology · 2020Article
- Dietary Restriction Suppresses Steatosis-Associated Hepatic Tumorigenesis in Hepatitis C Virus Core Gene Transgenic Mice.Liver cancer · 2020Article
- Celastrol ameliorates acute liver injury through modulation of PPARα.Biochemical pharmacology · 2020Article
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Authors and funding
10 authors at 2 institutions in 3 countries.
Funding
Abstract
Growth arrest and DNA damage-inducible 45 α (Gadd45α) is a stress-inducible protein that plays an important role in cell survival/death and DNA repair, but its contribution to the development of nonalcoholic steatohepatitis (NASH) has not been investigated. C57BL/6 Gadd45a-null and wild-type (WT) mice were treated with a methionine and choline-deficient diet (MCD) for eight weeks and phenotypic changes examined. Gadd45a-null mice had more severe hepatic inflammation and fibrosis, higher levels of mRNAs encoding pro-inflammatory, pro-fibrotic, and pro-apoptotic proteins, and greater oxidative and endoplasmic reticulum (ER) stress compared with WT mice. Indeed, Gadd45a mRNA was induced in response to ER stress in primary hepatocytes. Lipidomic analysis of NASH livers demonstrated decreased triacylglycerol (TG) in MCD-treated Gadd45a-null mice, which was associated with increased mRNAs encoding phospholipase D (Pld1/2), phosphatidic acid phosphatase type 2A, and choline/ethanolamine phosphotransferase 1 (Cept1), involved in the phosphatidylcholine-phosphatidic acid-diacylglycerol cycle, and decreased mRNAs encoding fatty acid (FA)-binding protein 1 (Fabp1) and FA transport protein 5. Treatment of cultured primary hepatocytes with tumor necrosis factor α, transforming growth factor β, and hydrogen peroxide led to the corresponding induction of Fabp1, Pld1/2, and Cept1 mRNAs. Collectively, Gadd45α plays protective roles against MCD-induced NASH likely due to attenuating cellular stress and ensuing inflammatory signaling. These results also suggest an interconnection between hepatocyte injury, inflammation and disrupted glycerophospholipid/FA metabolism that yields a possible mechanism for decreased TG accumulation with NASH progression (i.e., "burned-out" NASH).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.