PRDX1 (Peroxiredoxin 1)

Additionally, Rg5 not only suppresses HepG2 cell survival but also acts synergistically with doxorubicin, a first-line chemotherapeutic agent, to markedly enhance antitumor efficacy and potentially mitigate chemoresistance. Collectively, these findings suggest that PRDX1 inhibition may represent a broadly exploitable vulnerability in liver cancer and establish Rg5 as a promising candidate for developing targeted and combinatorial therapies against HCC.

In silico docking studies identified Leu583 as a key residue in Nrf2-ligand interactions. These findings suggest that Cannabis sativa L. polyphenols are key bioactive compounds modulating redox homeostasis and inflammation, and offering neuroprotective benefits with potential relevance in diseases involving mitochondrial dysfunction and oxidative damage.

Additionally, PRDX2 silencing inhibited growth of U87MG cells and increased the level of reactive oxygen species. Furthermore, such modulation reduced susceptibility to CONA, suggesting that this compound exerts its effect on cell viability at least partially through PRDX2 inhibition.

These findings identify Prdx1 as a potential therapeutic target for BLM-induced ALI, offering a strategy to mitigate its pulmonary toxicity and facilitate the broader clinical application of BLM.

This study revealed that Prdx1, Prdx2, Prdx4, and Prdx5 were elevated in depression models, which might relate to the occurrence of neuroinflammation, coupled with upregulation of oxidative stress responses. This study provided new strategies for the treatment of depression.

This multi-omics study illuminates the transcriptional and functional heterogeneity of TAMs in KIRC and establishes a macrophage-derived prognostic signature with translational potential. Our findings underscore the dual roles of macrophage polarization in mediating immune suppression and metabolic adaptation, offering novel targets for clinical diagnosis and treatment of KIRC.

Mechanistically, miR-27a-3p inhibited PPARγ, resulting in downregulation of PRDX1 and activation of the JNK pathway, which triggered oligodendrocyte apoptosis. These findings demonstrate that exosome-mediated delivery of miR-27a-3p antagomir mitigates SAH-induced WMI through modulation of the PPARγ/PRDX1/JNK axis, providing a promising noninvasive therapeutic approach for enhancing white matter repair and functional recovery after SAH.

Clinically, this work could support the development of EGCG-based interventions tailored to individual redox profiles, offering a precise chemopreventive strategy for patients at high risk of malignancies driven by metabolic and oxidative dysregulation. Furthermore, the identification of new genetic markers of EGCG sensitivity and resistance may inform future exploration of patient stratification.

Our study reveals that GBA harbors malignant potential at both epithelial and immune microenvironmental levels. The expression of CCL20, CCL5, and PRDX1 may serve as molecular markers for stratifying high-risk GBA, while PRDX1 represents a promising therapeutic target for reprogramming the tumor immune microenvironment in GBC.

This study identifies SLC25A39 as a novel oncogenic driver in HCC. By stabilizing PRDX1 and sustaining mitochondrial redox balance, SLC25A39 promotes tumor progression while preventing necroptotic cell death. Targeting the interplay between SLC25A39, PRDX1, and necroptotic signaling may provide new therapeutic opportunities for HCC.

However, questions remain regarding the upstream receptor for Prdx1, heterogeneity across CRC subtypes, and the balance between therapeutic benefit and inflammatory toxicity. By establishing Prdx1-induced pyroptosis as a driver of tumor suppression, this work advances a promising paradigm in CRC therapy, linking cell death to immune activation and pointing toward future biomarker-driven, pyroptosis-based interventions.

This study classified BC by mRNAsi-related genes and established corresponding risk models. The findings of the present study propose a novel classification tool based on stem cell characteristics, which has the potential to be employed for prognostic stratification in BC patients and to offer guidance for developing personalised treatment strategies.