ArticleThe Journal of biological chemistry2015
Estrogen Sulfotransferase Is an Oxidative Stress-responsive Gene That Gender-specifically Affects Liver Ischemia/Reperfusion Injury.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Estrogen sulfotransferase in the metabolism of estrogenic drugs and in the pathogenesis of diseases.Expert opinion on drug metabolism & toxicology · 2019Pooled it
- Protective effects ofRedox report : communications in free radical research · 2026Article
- Protocol for surgical stress-promoted colorectal cancer liver metastasis in mice.STAR protocols · 2026Article
- Article
- Transcriptional insights into aflatoxin B1 induced hepatotoxicity and comparative effects of medicinal herbs in pigs.BMC veterinary research · 2026Article
- The effects of short-chain fatty acids on androstenone metabolism in porcine hepatocytes.Journal of animal science · 2026Article
- Liver-specific glucocorticoid action in alcoholic liver disease: Study of glucocorticoid receptor knockout and knockin mice.Liver research (Beijing, China) · 2024Article
- Estrogen sulfotransferase and sulfatase in steroid homeostasis, metabolic disease, and cancer.Steroids · 2024Review
- Dialyl-sulfide with trans-chalcone prevent breast cancer prohibiting SULT1E1 malregulations and oxidant-stress induced HIF1a-MMPs induction.Genes & cancer · 2024Article
- Sex differences in hepatic ischemia‒reperfusion injury: a cross-sectional study.Scientific reports · 2023Article
- Sex-specific expression mechanism of hepatic estrogen inactivating enzyme and transporters in diabetic women.Biochemical pharmacology · 2021Article
- RNA-Seq Reveals Different Gene Expression in Liver-Specific Prohibitin 1 Knock-Out Mice.Frontiers in physiology · 2021Article
- Eicosanoid production varies by sex in mesenteric ischemia reperfusion injury.Clinical immunology (Orlando, Fla.) · 2020Article
- RORα phosphorylation by casein kinase 1α as glucose signal to regulate estrogen sulfation in human liver cells.The Biochemical journal · 2020Article
- The Role of Sulfotransferases in Liver Diseases.Drug metabolism and disposition: the biological fate of chemicals · 2020Review
- BPA disrupts 17‑estradiol‑mediated hepatic protection against ischemia/reperfusion injury in rat liver by upregulating the Ang II/AT1R signaling pathway.Molecular medicine reports · 2020Article
- Inhibition of Estrogen Sulfotransferase (Journal of the American Society of Nephrology : JASN · 2020Article
- Dependence between estrogen sulfotransferase (SULT1E1) and nuclear transcription factor Nrf-2 regulations via oxidative stress in breast cancer.Molecular biology reports · 2020Review
- Breast cancer pathogenesis is linked to the intra-tumoral estrogen sulfotransferase (hSULT1E1) expressions regulated by cellular redox dependent Nrf-2/NFCancer cell international · 2020Article
- Hepatic Estrogen Sulfotransferase Distantly Sensitizes Mice to Hemorrhagic Shock-Induced Acute Lung Injury.Endocrinology · 2020Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Estrogen sulfotransferase (EST) regulates estrogen homeostasis by sulfonating and deactivating estrogens. Liver ischemia and reperfusion (I/R) involves both hypoxia during the ischemic phase and oxidative damage during the reperfusion phase. In this report, we showed that the expression of EST was markedly induced by I/R. Mechanistically, oxidative stress-induced activation of Nrf2 was responsible for the EST induction, which was abolished in Nrf2(-/-) mice. EST is a direct transcriptional target of Nrf2. In female mice, the I/R-responsive induction of EST compromised estrogen activity. EST ablation attenuated I/R injury as a result of decreased estrogen deprivation, whereas this benefit was abolished upon ovariectomy. The effect of EST ablation was sex-specific because the EST(-/-) males showed heightened I/R injury. Reciprocally, both estrogens and EST regulate the expression and activity of Nrf2. Estrogen deprivation by ovariectomy abolished the I/R-responsive Nrf2 accumulation, whereas the compromised estrogen deprivation in EST(-/-) mice was associated with increased Nrf2 accumulation. Our results suggested a novel I/R-responsive feedback mechanism to limit the activity of Nrf2 in which Nrf2 induces the expression of EST, which subsequently increases estrogen deactivation and limits the estrogen-responsive activation of Nrf2. Inhibition of EST, at least in females, may represent an effective approach to manage hepatic I/R injury.
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Registered trials
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