The good Samaritan glutathione-S-transferase P1: An evolving relationship in nitric oxide metabolism mediated by the direct interactions between multiple effector molecules

Russell, Tiffany M.; Richardson, Des R.

doi:10.1016/j.redox.2022.102568

Cited by 13 publications

(7 citation statements)

References 219 publications

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“…Through interactions with IKK, GSTP1 can suppress NFκB signaling. This reduces iNOS expression and stimulates apoptosis, which controls NO-mediated ROS production 123 . By blocking the p38 MAPK/ NFκB pathway, cathepsin C downregulation improves HUVEC function.…”

Section: Nfκb Signaling Influences Pe Developmentmentioning

confidence: 99%

The NFκB Signaling Pathway Is Involved in the Pathophysiological Process of Preeclampsia

Li,

Zhu,

et al. 2024

Geburtshilfe Frauenheilkd

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The high prevalence of preeclampsia (PE) is a major cause of maternal and fetal mortality and affects the long-term prognosis of both mother and baby. Termination of pregnancy is currently the only effective treatment for PE, so there is an urgent need for research into its pathogenesis and the development of new therapeutic approaches. The NFκB family of transcription factors has an essential role in inflammation and innate immunity. In this review, we summarize the role of NFκB in normal and preeclampsia pregnancies, the role of NFκB in existing treatment strategies, and potential NFκB treatment strategies.

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Section: Nfκb Signaling Influences Pe Developmentmentioning

confidence: 99%

The NFκB Signaling Pathway Is Involved in the Pathophysiological Process of Preeclampsia

Li,

Zhu,

et al. 2024

Geburtshilfe Frauenheilkd

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“…Glutathione (GSH) is the key intracellular antioxidant molecule that is almost completely reduced in normal condition: the ratio of oxidized/reduced GSH is considered to be a reliable indicator of intracellular oxidation [8,9]. Glutathione S-transferases (GSTs)are a superfamily of detoxifying enzymes that protect cells from any oxidative stress deriving from inflammation and from the environment by catalyzing the reaction of reduced GSH with oxidants [11].Catalase and Superoxide Dismutase2(SOD2) are mitochondrial antioxidant enzymes involved in intracellular detoxification: SOD2 transforms superoxide O ° into hydrogen peroxide (H2O2) and diatomic oxygen, Catalase decomposes H2O2 into water and oxygen and completes the detoxifying cycle [12]. Upon activation of mitochondrial oxidative pathways, SOD is released from mitochondria and externalized by cytoskeletal remodelling [13,14].…”

Section: Oxidative Systemsmentioning

confidence: 99%

Mechanisms Limiting Renal Tissue Protection and Repair in Glomerulonephritis

Angeletti,

Bruschi,

Kajana

et al. 2023

IJMS

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Glomerulonephritis are renal disorders resulting from different pathogenic mechanisms (i.e., autoimmunity, complement, inflammatory activation, etc.). Clarifying details of the pathogenic cascade is basic to limit the progression from starting inflammation to degenerative stages. The balance between tissue injury, activation of protective systems and renal tissue repair determines the final outcome. Induction of an oxidative stress is part of glomerular inflammation and activation of protective antioxidant systems has a crucial role in reducing tissue effects. The generation of highly reactive oxygen species can be evaluated in vivo by tracing the inner-layer content of phosphatidyl ethanolamine and phosphatidyl serine in cell membranes. Albumin is the major antioxidant in serum and the level of oxidized albumin is another indirect sign of oxidative stress. Studies performed in Gn, specifically in FSGS, showed a high degree of oxidation in most contexts. High levels of circulating anti-SOD2 antibodies, limiting the detoxyfing activity of SOD2, have been detected in autoimmune Gn(lupus nephritis and membranous nephropathy) in association with persistence of proteinuria and worsening of renal function. In renal transplant, high levels of circulating anti-Glutathione S-transferase antibodies have been correlated with chronic antibody rejection and progressive loss of renal function. Annexins, mainly ANXA1 and ANXA2, play a general anti-inflammatory effect by inhibiting neutrophil functions. Cytosolic ANXA1 is decreased in apoptotic neutrophils of patients with glomerular polyangitis in association with delayed apoptosis that is considered the mechanism for polyangitis. High circulating levels of anti-ANXA1 and anti-ANXA2 antibodies characterize lupus nephritis implying a reduced anti-inflammatory effect. High circulating levels of antibodies targeting Macrophages (anti-FMNL1) have been detected in Gn in association with proteinuria. They potentially modify the intra-glomerular presence of protective macrophages (M2a, M2c) thus acting on the composition of renal infiltrate and on tissue repair.

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“…It is involved in apoptosis resistance and metabolism of various chemotherapeutic agents, such as platinum-based drugs [ 16 , 17 ]. In addition, hGSTP1-1 regulates calcium channels by reducing the apoptotic mobilization of calcium ions [ 18 ] and modulating the function of apoptotic signalling of JNK1 [ 19 , 20 ] and Bax [ 21 ]. Additionally, hGSTP1-1 regulates calcium channels by reducing the apoptotic mobilization of calcium ions [ 18 ], modulating the function of apoptotic signalling of JNK1 [ 19 , 20 ] and Bax [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

“…In addition, hGSTP1-1 regulates calcium channels by reducing the apoptotic mobilization of calcium ions [ 18 ] and modulating the function of apoptotic signalling of JNK1 [ 19 , 20 ] and Bax [ 21 ]. Additionally, hGSTP1-1 regulates calcium channels by reducing the apoptotic mobilization of calcium ions [ 18 ], modulating the function of apoptotic signalling of JNK1 [ 19 , 20 ] and Bax [ 21 ]. The regulation of tumor necrosis factor (TNF), TNF-receptor factor 2 (TRAF2), and apoptosis signal-regulating kinase 1 (ASK1) is another crucial function of hGSTP1-1 [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

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Inhibition Analysis and High-Resolution Crystal Structure of Mus musculus Glutathione Transferase P1-1

et al. 2023

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Multidrug resistance is a significant barrier that makes anticancer therapies less effective. Glutathione transferases (GSTs) are involved in multidrug resistance mechanisms and play a significant part in the metabolism of alkylating anticancer drugs. The purpose of this study was to screen and select a lead compound with high inhibitory potency against the isoenzyme GSTP1-1 from Mus musculus (MmGSTP1-1). The lead compound was selected following the screening of a library of currently approved and registered pesticides that belong to different chemical classes. The results showed that the fungicide iprodione [3-(3,5-dichlorophenyl)-2,4-dioxo-N-propan-2-ylimidazolidine-1-carboxamide] exhibited the highest inhibition potency (ΙC50 = 11.3 ± 0.5 μΜ) towards MmGSTP1-1. Kinetics analysis revealed that iprodione functions as a mixed-type inhibitor towards glutathione (GSH) and non-competitive inhibitor towards 1-chloro-2,4-dinitrobenzene (CDNB). X-ray crystallography was used to determine the crystal structure of MmGSTP1-1 at 1.28 Å resolution as a complex with S-(p-nitrobenzyl)glutathione (Nb-GSH). The crystal structure was used to map the ligand-binding site of MmGSTP1-1 and to provide structural data of the interaction of the enzyme with iprodione using molecular docking. The results of this study shed light on the inhibition mechanism of MmGSTP1-1 and provide a new compound as a potential lead structure for future drug/inhibitor development.

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The good Samaritan glutathione-S-transferase P1: An evolving relationship in nitric oxide metabolism mediated by the direct interactions between multiple effector molecules

Cited by 13 publications

References 219 publications

The NFκB Signaling Pathway Is Involved in the Pathophysiological Process of Preeclampsia

The NFκB Signaling Pathway Is Involved in the Pathophysiological Process of Preeclampsia

Mechanisms Limiting Renal Tissue Protection and Repair in Glomerulonephritis

Inhibition Analysis and High-Resolution Crystal Structure of Mus musculus Glutathione Transferase P1-1

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