GSTA1

更新于：2025-05-07

基本信息

别名

13-hydroperoxyoctadecadienoate peroxidase、Androst-5-ene-3,17-dione isomerase、Glutathione S-transferase A1

+ [8]

简介

Glutathione S-transferase that catalyzes the nucleophilic attack of the sulfur atom of glutathione on the electrophilic groups of a wide range of exogenous and endogenous compounds (Probable). Involved in the formation of glutathione conjugates of both prostaglandin A2 (PGA2) and prostaglandin J2 (PGJ2) (PubMed:9084911). It also catalyzes the isomerization of D5-androstene-3,17-dione (AD) into D4-androstene-3,17-dione and may therefore play an important role in hormone biosynthesis (PubMed:11152686). Through its glutathione-dependent peroxidase activity toward the fatty acid hydroperoxide (13S)-hydroperoxy-(9Z,11E)-octadecadienoate/13-HPODE it is also involved in the metabolism of oxidized linoleic acid (PubMed:16624487).

关联

100 项与 GSTA1 相关的临床结果

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100 项与 GSTA1 相关的转化医学

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0 项与 GSTA1 相关的专利（医药）

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1,254

项与 GSTA1 相关的文献（医药）

2025-05-01·Archives of Gerontology and Geriatrics

Unraveling the protein-metabolite network of sarcopenia in plasma: A large-scale Mendelian randomization study

Article

作者: Guo, Wen ; Zuo, Wenhang ; Wu, Jinhui ; Peng, Jin

BACKGROUNDSome plasma molecules may have an effect on sarcopenia, but it is not fully understood. We aimed to comprehensively explore the causal effects of plasma proteins and metabolites on sarcopenia traits, and to unravel their network.METHODSA two-sample Mendelian randomization design was adopted. The levels of 4,907 plasma proteins from 35,559 Icelanders, and 1,400 plasma metabolites from 8,299 Europeans, were set as exposures. Low handgrip strength, appendicular lean mass, and usual walking pace from Europeans were set as outcomes. Inverse-variance weighted (IVW) and four other methods, along with sensitivity analyzes, were performed to estimate the causal effects. Enrichment and pathway analyzes were conducted to present their characteristics. IVW was used to estimate the bidirectional relationships between sarcopenia-related proteins and metabolites, and to visualize them within a network.RESULTSWe identified 76 relationships between proteins and sarcopenia traits. The absolute values of causal effects (β_IVW) ranging from 0.01 to 0.35. IL2, AIF1, GDNF, CXCL13, LRRTM3, and SLPI were the top six proteins ranked by causal effects. Additionally, 22 relationships between metabolites and sarcopenia traits were identified, with absolute values of β_IVW ranging from 0.02 to 0.22. Sulfate and serine/pyruvate ratio had the highest values. The network diagram showed some key nodes, such as ISOC1, GSTA1, tryptophan and 5α-androstan-3α,17β-diol monosulfate.CONCLUSIONSThis work unraveled a molecular network of sarcopenia in plasma for the first time and identified some key proteins and metabolites. It may help to understand the mechanisms of sarcopenia, providing new insights for predicting, diagnosing and treating sarcopenia.

2025-03-01·Internal and Emergency Medicine

Precision medicine in intestinal ischemia: the emerging role of biomarkers

Review

作者: Liberale, Luca ; Olivero, Chiara ; Carbone, Federico ; Montecucco, Fabrizio

Intestinal ischemia (IIs) is a significant gastrointestinal condition characterized by reduced blood flow to the bowel, leading to inflammation and injury. Early diagnosis and management are crucial for preventing severe complications. Under this point of view, circulating biomarkers can enhance patient stratification and guide therapeutic decisions. Fatty acid-binding proteins (FABPs), specifically I-FABP and L-FABP, are small cytosolic proteins released upon enterocyte membrane integrity loss, with elevated plasma levels indicating early intestinal ischemia. Stromal Cell-Derived Factor-1 (SDF-1) regulates stem cell function and shows significantly higher levels in patients with IIs and cardiovascular disease compared to controls. D-Lactate, a bacterial fermentation byproduct, is another significant marker, with higher serum levels observed in intestinal ischemia cases. Alpha-glutathione S-transferase combats intracellular oxidative stress, with significantly elevated levels in acute mesenteric ischemia patients. Additionally, SM22, a small smooth muscle protein, shows higher plasma levels in patients with transmural ischemia compared to those with mucosal ischemic lesions and healthy controls. These biomarkers are promising for their roles in early detection and differentiation of IIs from other gastrointestinal conditions. Therapeutic strategies, including anti-inflammatory therapies, have shown efficacy in managing IIs symptoms and preventing recurrence. This review aims to inform clinicians and researchers about the current advancements in biomarker research and therapeutic approaches for IIs, emphasizing the importance of integrating these biomarkers and treatments into clinical practice to improve the management and prognosis of the disease.

2025-03-01·Journal of Hazardous Materials

Effects of mixed exposure to PFAS on adolescent non-alcoholic fatty liver disease: Integrating evidence from human cohorts, toxicogenomics, and animal models to uncover mechanisms and potential target sites

Article

作者: Qian, Kelei ; Gao, Liping ; Xu, Xueming ; Li, Dan-Lin ; Pan, Chen-Wei ; Zheng, Ya-Jie ; Du, Xiushuai ; Zheng, Weiwei ; Li, Yue-Zu ; Du, Zhiyuan ; Wu, Yitian ; Tao, Gonghua ; Qin, Yu ; Xu, Jing ; Liang, Gang

Extensive evidence suggests a correlation between environmental pollutants, specifically perfluoroalkyl and polyfluoroalkyl substances (PFAS) and non-alcoholic fatty liver disease (NAFLD). This study aims to investigate the association and underlying mechanisms of PFAS-induced NAFLD in adolescents by employing a comprehensive approach of population-based studies, toxicogenomics, and animal models. A total of 2014 freshmen from Dali University were recruited for this study, with 1694 participants undergoing serum testing for PFAS exposure. Additionally, Comparative Toxicogenomics Database analysis and PFAS exposure experiments were conducted by orally administering PFAS to 8-week-old adult C57/6 J mice for 28 days. Epidemiological analysis of the adolescent cohort revealed that perfluorohexanesulfonic acid and perfluorooctanoic acid are significant risk factors for NAFLD in adolescents. Toxicogenomic analysis revealed that the negative regulation of gap junction assembly and glutathione derivative biosynthesis contributes to NAFLD development. Animal model studies further demonstrated that combined PFAS exposure led to pathological changes in hepatocytes, including inflammation and steatosis, elevated liver enzymes, cholestasis, and bile canalicular blockage. This study reveals that PFAS exposure serves as a significant risk factor for hepatic steatosis/NAFLD in adolescents. The activation of cytochrome P4502E1 and glutathione S-transferase A1 signaling highlights new molecular targets for PFAS-induced disruptions in hepatic lipid metabolism.

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