GLRX (Glutaredoxin)

This study constructed and validated a metabolism-driven prognostic model. The model enables prognostic stratification of LGG patients and links high-risk scores to metabolic dysregulation and an immunosuppressive microenvironment characterized by M2 macrophage enrichment, based on multi-omics data. Mechanistic exploration indicates this association is particularly pronounced in myeloid cells, predominantly within metabolism-related M2 macrophage subpopulations. Furthermore, computational analysis suggests differences in drug sensitivity between risk groups and identifies potential therapeutic compounds, providing clues for future exploration of therapeutic strategies targeting metabolic-immune interactions.

Crucially, upon Nrf2 knockdown in HLEB3 cells via short interfering RNA, SSP confirmed its protective role by activating Nrf2 to inhibite apoptosis and ferroptosis. Collectively, these findings demonstrate that SSP protects LECs against HG-induced damage through Nrf2-mediated coordination of antioxidant defense, anti-apoptotic, and anti-ferroptotic mechanisms, highlighting its therapeutic potential for DC.

Moreover, both genetic and pharmacologic inhibition of mPTP opening restored the leukemic potential of primary AML specimens in the absence of GLRX2. By disrupting glutathionylation-dependent mitochondrial homeostasis, this study reveals a novel vulnerability in AML that could inform future therapeutic strategies.

Grx2 acts as a redox checkpoint that limits ABC-driven autoimmunity by modulating ROS. The Grx2-ROS axis represents a potential therapeutic target for SLE and related chronic inflammatory diseases.

Our results showed that the TT genotype of rs912071 is associated with an increased risk of recurrence and high oxidative stress. In contrast, the CT genotype may protect against disease recurrence in patients with UBC cancer.

Treatment of the Huh-7 and HepG2 cells exposed to fructose with ursodeoxycholic acid (UDCA) or its taurine-conjugated form, TUDCA, which are known to elicit protective hepatocellular effects by inducing antioxidant defenses, strongly inhibited succinate build up by preserving mitochondrial function and preventing H2O2 hyper-production. Collectively, our findings show succinate accumulates rapidly in the extracellular milieu in our mouse model for MASLD and cell culture models for hepatic lipotoxicity. These findings suggest the applicability of succinate as a biomarker of early MASLD particularly among males and especially in pediatric populations.

The present review summarizes, for the first time, at least to the best of our knowledge, the association of SSG with distinct PCD subtypes, and highlights therapeutic strategies targeting GRX activity or site-specific SSG modulation (e.g., pyruvate kinase M2 Cys423/424). Emerging approaches, including GRX mimetics and thiol-targeted drugs, hold promise for precision medicine in redox-related pathologies.

Thus, we highlighted several enzymatic antioxidant components, such as superoxide dismutase, catalase, heme oxygenase-1, peroxiredoxin, glutaredoxin, thioredoxin, thioredoxin reductase, glutathione peroxidase, and antioxidant components, including glutathione, nuclear factor erythroid 2-related factor 2, 8-oxo-7,8-dihydro-2'-deoxyguanosine, and mitochondrial citrate carrier SLC25A1, based on PubMed and Scopus-indexed literature. Understanding the oxidative stress defense system in lung cancer would be beneficial for developing and expanding therapeutic strategies, such as drug development, drug design, and advanced delivery platforms.

Grx2 plays an oncogenic role in colon cancer cells and also affects the relapse-free survival of patients with colon cancer. Grx2 may be a novel prognostic biomarker and therapeutic target for colon cancer.

Given the gravity of the situation and to look at the bigger picture of 'trans-S-nitrosylation', we aim to present a novel attempt at justifying the hesitance in accepting antioxidants as capable of transnitrosylating their cognate protein partners and reflecting on the need to resolve the controversy that would be crucial from the perspective of understanding therapeutic outcomes involving such cellular antioxidants in disease pathogenesis. Further characterization is required to identify the regulatory mechanisms or conditions where an antioxidant like Trx, Grx, or DJ-1 can act as a cellular transnitrosylase.