ArticleAntioxidants (Basel, Switzerland)2019
Inhibition of Heme Oxygenase Antioxidant Activity Exacerbates Hepatic Steatosis and Fibrosis
Article in Antioxidants (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Stage-specific role of IGFBP-3/TMEM219 pathway in liver fibrosis progression using a bile duct ligation rat model.Molecular biology reports · 2025Article
- Investigation of HO-1 Regulation of Liver Fibrosis Related to Nonalcoholic Fatty Liver Disease Through the SIRT1/TGF-ß/Smad3 Pathway.Journal of clinical and translational hepatology · 2025Article
- Red Oranges and Olive Leaf Waste-Derived Bioactive Extracts Promote Adipocyte Functionality In Vitro.Nutrients · 2024Article
- Synthetic biology approach revealed enhancement in haeme oxygenase-1 gene expression by codon pair optimization while reduction by codon deoptimization.Annals of medicine and surgery (2012) · 2024Article
- Association between heme oxygenase-1 and hyperlipidemia in pre-diabetic patients: a cross-sectional study.Frontiers in endocrinology · 2024Observational
- Heme oxygenase-1 mitigates liver injury and fibrosis via modulation of LNX1/Notch1 pathway in myeloid cells.iScience · 2022Article
- Beneficial Effects of Standardized Extracts from Wastes of Red Oranges and Olive Leaves.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- The effect of endurance training on non-alcoholic fatty liver disease in mice.Physiological reports · 2021Article
- Novel Heme Oxygenase-1 (HO-1) Inducers Based on Dimethyl Fumarate Structure.International journal of molecular sciences · 2020Article
- Natural Product Heme Oxygenase Inducers as Treatment for Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2020Review
- Modulation of Pro-Oxidant and Pro-Inflammatory Activities of M1 Macrophages by the Natural Dipeptide Carnosine.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The progression of non-alcoholic fatty liver disease (NAFLD) and the development of hepatic fibrosis is caused by changes in redox balance, leading to an increase of reactive oxygen species (ROS) levels. NAFLD patients are at risk of progressing to non-alcoholic steatohepatitis (NASH), associated to cardiovascular diseases (CVD), coronary heart disease and stroke. Heme Oxygenase-1 (HO-1) is a potent endogenous antioxidant gene that plays a key role in decreasing oxidative stress. The present work was directed to determine whether use of an inhibitor of HO-1 activity affects lipid metabolism and fibrosis process in hepatic cells. Oil Red assay and mRNA analysis were used to evaluate the triglycerides content and the lipid metabolism pathway in HepG2 cells. ROS measurement, RT-PCR and Soluble collagen assay were used to assess the intracellular oxidant, the fibrosis pathway and the soluble collagen in LX2 cells. The activity of HO-1 was inhibited using Tin Mesoporphyrin IX (SnMP). Our study demonstrates that a non-functional HO system results in an increased lipid storage and collagen release in hepatocytes. Consequently, an increase of HO-1 levels may provide a therapeutic approach to address the metabolic alterations associated with NAFLD and its progression to NASH.
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Registered trials
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 Socratic graph.