ArticleInternational journal of physiology, pathophysiology and pharmacology2016
The mitochondria-targeted antioxidant MitoQ attenuates liver fibrosis in mice.
Article in International journal of physiology, pathophysiology and pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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Who cites it
47 citing papers in PubMed, 69 citations in OpenAlex.
- Hydrogen peroxide sensing and signaling in physiology and disease: implications for therapy.Signal transduction and targeted therapy · 2026Review
- Role of Acetaldehyde and Dysregulated Mitophagic Lysosomal Processing in Chronic-Binge Ethanol-Induced Liver Injury.International journal of molecular sciences · 2025Article
- Regulatory role of vitamin DScientific reports · 2025Article
- Evaluating the mitochondrial structure and gene expression profile of regenerated liver tissues in mice after 85% partial hepatectomy.Journal of gastrointestinal oncology · 2024Article
- Mitochondria-Targeted Antioxidant MitoQ Improves In Vitro Maturation and Subsequent Embryonic Development from Culled Cows.Animals : an open access journal from MDPI · 2024Article
- LP340, a novel histone deacetylase inhibitor, decreases liver injury and fibrosis in mice: role of oxidative stress and microRNA-23a.Frontiers in pharmacology · 2024Article
- Contribution of Mitochondrial Reactive Oxygen Species to Chronic Hypoxia-Induced Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023Article
- Cellular stress in the pathogenesis of nonalcoholic steatohepatitis and liver fibrosis.Nature reviews. Gastroenterology & hepatology · 2023Review
- Article
- Reduced Lipid Peroxidation Predicts Unfavorable Prognosis in Hepatocellular Carcinoma, but Not Intrahepatic Cholangiocarcinoma.Biomedicines · 2023Article
- Novel Therapeutic Approaches to Liver Fibrosis Based on Targeting Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Review
- Therapeutic interventions of acute and chronic liver disorders: A comprehensive review.World journal of hepatology · 2023Review
- MitoQ alleviates carbon tetrachloride-induced liver fibrosis in mice through regulating JNK/YAP pathway.Toxicology research · 2022Article
- Mitoquinol mesylate (MITOQ) attenuates diethyl nitrosamine-induced hepatocellular carcinoma through modulation of mitochondrial antioxidant defense systems.Toxicological research · 2022Article
- Is Mitochondrial Oxidative Stress a Viable Therapeutic Target in Preeclampsia?Antioxidants (Basel, Switzerland) · 2022Review
- Mitochondrial Dysfunction and Oxidative Stress in Liver Transplantation and Underlying Diseases: New Insights and Therapeutics.Transplantation · 2021Review
- Systemic delivery of a mitochondria targeted antioxidant partially preserves limb muscle mass and grip strength in response to androgen deprivation.Molecular and cellular endocrinology · 2021Article
- Anthelmintic Activity of Antioxidants: In Vitro Effects on the Liver FlukePathogens (Basel, Switzerland) · 2021Article
- Long non-coding RNAs: Promising new targets in pulmonary fibrosis.The journal of gene medicine · 2021Review
- Effect of mitoquinone on liver metabolism and steatosis in obese and diabetic rats.Pharmacology research & perspectives · 2021Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
Abstract
Oxidative stress plays an essential role in liver fibrosis. This study investigated whether MitoQ, an orally active mitochondrial antioxidant, decreases liver fibrosis. Mice were injected with corn oil or carbon tetrachloride (CCl4, 1:3 dilution in corn oil; 1 µl/g, ip) once every 3 days for up to 6 weeks. 4-Hydroxynonenal adducts increased markedly after CCl4 treatment, indicating oxidative stress. MitoQ attenuated oxidative stress after CCl4. Collagen 1α1 mRNA and hydroxyproline increased markedly after CCl4 treatment, indicating increased collagen formation and deposition. CCl4 caused overt pericentral fibrosis as revealed by both the sirius red staining and second harmonic generation microscopy. MitoQ blunted fibrosis after CCl4. Profibrotic transforming growth factor-β1 (TGF-β1) mRNA and expression of smooth muscle α-actin, an indicator of hepatic stellate cell (HSC) activation, increased markedly after CCl4 treatment. Smad 2/3, the major mediator of TGF-β fibrogenic effects, was also activated after CCl4 treatment. MitoQ blunted HSC activation, TGF-β expression, and Smad2/3 activation after CCl4 treatment. MitoQ also decreased necrosis, apoptosis and inflammation after CCl4 treatment. In cultured HSCs, MitoQ decreased oxidative stress, inhibited HSC activation, TGF-β1 expression, Smad2/3 activation, and extracellular signal-regulated protein kinase activation. Taken together, these data indicate that mitochondrial reactive oxygen species play an important role in liver fibrosis and that mitochondria-targeted antioxidants are promising potential therapies for prevention and treatment of liver fibrosis.
Indexed as
Identifiers
27186319PMC4859875W2406284904What OpenQuestion holds
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 OpenQuestion graph.