ArticleCell death & disease2025
Estrogen-dependent activation of TRX2 reverses oxidative stress and metabolic dysfunction associated with steatotic disease.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Protective effects ofRedox report : communications in free radical research · 2026Article
- The regulation of intrahepatic fatty acid partitioning within the human liver: the effect of sex.Clinical science (London, England : 1979) · 2026Review
- Article
- Myeloid monoamine oxidase A protects against glucose intolerance, insulin resistance and weight gain in high-fat diet-fed mice by preventing the hyperactivation of macrophages.The Journal of nutritional biochemistry · 2026Article
- ATP6V1B2 alleviates hepatic steatosis by promoting lysosomal acidification in hepatocytes.Cell death discovery · 2026Article
- Association of pregnancy history and unhealthy lifestyle with biological age acceleration: a large cross-sectional study.Frontiers in public health · 2026Article
- Hematopoietic monoamine oxidase A deficiency exacerbates neuroinflammation and demyelination in female but not male mice with experimental autoimmune encephalomyelitis.Frontiers in immunology · 2026Article
- Cadmium exposure during adolescence and young adulthood induces signatures of metabolic dysfunction-associated steatotic liver disease.Scientific reports · 2025Article
- Genome-Wide Thioredoxin System inBiology · 2025Article
- CD44 and SLC1A2 are commonly regulated but do not form a fusion transcript in ER+ breast cancer.Molecular and cellular biochemistry · 2025Article
- In Situ Assembly of Fluorogenic RNA for Screening Natural Anti-Liver Fibrosis Products via Dynamic Visualization of COL1A1 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Structural and systems characterization of phosphorylation on metabolic enzymes identifies sex-specific metabolic reprogramming in obesity.Molecular cell · 2025Article
- Possible association between metabolic dysfunction-associated steatotic liver disease predictors and hand grip strength.Scientific reports · 2025Article
- Article
- Association between polycyclic aromatic hydrocarbons exposure and metabolic dysfunction-associated steatotic liver disease in US adults.Frontiers in public health · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) encompasses a spectrum of hepatic disorders, ranging from simple steatosis to steatohepatitis, with the most severe outcomes including cirrhosis, liver failure, and hepatocellular carcinoma. Notably, MASLD prevalence is lower in premenopausal women than in men, suggesting a potential protective role of estrogens in mitigating disease onset and progression. In this study, we utilized preclinical in vitro models-immortalized cell lines and hepatocyte-like cells derived from human embryonic stem cells-exposed to clinically relevant steatotic-inducing agents. These exposures led to lipid droplet (LD) accumulation, increased reactive oxygen species (ROS) levels, and mitochondrial dysfunction, along with decreased expression of markers associated with hepatocyte functionality and differentiation. Estrogen treatment in steatotic-induced liver cells resulted in reduced ROS levels and LD content while preserving mitochondrial integrity, mediated by the upregulation of mitochondrial thioredoxin 2 (TRX2), an antioxidant system regulated by the estrogen receptor. Furthermore, disruption of TRX2, either pharmacologically using auranofin or through genetic interference, was sufficient to counteract the protective effects of estrogens, highlighting a potential mechanism through which estrogens may prevent or slow MASLD progression.
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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 Socratic graph.