ArticleThe American journal of pathology2009
Protection against hepatocyte mitochondrial dysfunction delays fibrosis progression in mice.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 64 citations in OpenAlex.
- Chronic Exposure to Arsenic and Fluoride Starting at Gestation Alters Liver Mitochondrial Protein Expression and Induces Early Onset of Liver Fibrosis in Male Mouse Offspring.Biological trace element research · 2025Article
- Liver iron stores and effectors of ferroptosis are dependent on age and sex.Experimental physiology · 2024Article
- Cellular stress in the pathogenesis of nonalcoholic steatohepatitis and liver fibrosis.Nature reviews. Gastroenterology & hepatology · 2023Review
- Riboflavin ameliorates mitochondrial dysfunction via the AMPK/PGC1α/HO‑1 signaling pathway and attenuates carbon tetrachloride‑induced liver fibrosis in rats.Experimental and therapeutic medicine · 2022Article
- Cell non-autonomous effect of hepatic growth differentiation factor 15 on the thyroid gland.Frontiers in endocrinology · 2022Article
- Review
- NADPH oxidases: Pathophysiology and therapeutic potential in age-associated pulmonary fibrosis.Redox biology · 2020Review
- Mitochondrial stress protein HSP60 regulates ER stress-induced hepatic lipogenesis.Journal of molecular endocrinology · 2020Article
- Mitochondrial dysfunction in fibrotic diseases.Cell death discovery · 2020Review
- Article
- Fibroblast senescence in the pathology of idiopathic pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2018Review
- Possible Involvement of Mitochondrial Dysfunction and Oxidative Stress in a Cellular Model of NAFLD Progression Induced by Benzo[a]pyrene/Ethanol CoExposure.Oxidative medicine and cellular longevity · 2018Article
- GDF15 deficiency exacerbates chronic alcohol- and carbon tetrachloride-induced liver injury.Scientific reports · 2017Article
- Role of nonalcoholic fatty liver disease as risk factor for drug-induced hepatotoxicity.Journal of clinical and translational research · 2017Article
- Toxicological Implications of Mitochondrial Localization of CYP2E1.Toxicology research · 2017Article
- Citrate functionalized MnFuture science OA · 2016Article
- Roux-En Y Gastric Bypass Results in Long-Term Remission of Hepatocyte Apoptosis and Hepatic Histological Features of Non-alcoholic Steatohepatitis.Frontiers in physiology · 2016Article
- Circulating mitochondrial DNA content associated with the risk of liver cirrhosis: a nested case-control study.Digestive diseases and sciences · 2015Article
- Turnover rates of hepatic collagen and circulating collagen-associated proteins in humans with chronic liver disease.PloS one · 2015Article
- Targeting mitochondria as therapeutic strategy for metabolic disorders.TheScientificWorldJournal · 2014Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulating evidence indicates that oxidative stress is involved in the physiopathology of liver fibrogenesis. However, amid the global context of hepatic oxidative stress, the specific role of hepatocyte mitochondrial dysfunction in the fibrogenic process is still unknown. The aim of this study was to determine whether a targeted protection of hepatocytes against mitochondrial dysfunction could modulate fibrosis progression. We induced liver fibrogenesis by chronic carbon tetrachloride treatment (3 or 6 weeks of biweekly injections) in transgenic mice expressing Bcl-2 in their hepatocytes or in normal control mice. Analyses of mitochondrial DNA, respiratory chain complexes, and lipid peroxidation showed that Bcl-2 transgenic animals were protected against mitochondrial dysfunction and oxidative stress resulting from carbon tetrachloride injury. Picrosirius red staining, alpha-smooth muscle actin immunohistochemistry, and real-time PCR for transforming growth factor-beta and collagen alpha-I revealed that Bcl-2 transgenic mice presented reduced fibrosis at early stages of fibrogenesis. However, at later stages increased nonmitochondrial/nonhepatocytic oxidative stress eventually overcame the capacity of Bcl-2 overexpression to prevent the fibrotic process. In conclusion, we demonstrate for the first time that specific protection against hepatocyte mitochondrial dysfunction plays a preventive role in early stages of fibrogenesis, delaying its onset. However, with the persistence of the aggression, this protection is no longer sufficient to impede fibrosis progression.
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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 OpenQuestion graph.