Redox homeostasis and inflammation in fibroblasts of patients with Friedreich Ataxia: a possible cross talk DOI Creative Commons
Andrea Quatrana, Sara Petrillo,

Caterina Torda

и другие.

Frontiers in Molecular Neuroscience, Год журнала: 2025, Номер 18

Опубликована: Апрель 16, 2025

Redox homeostasis is impaired in Friedreich’s Ataxia (FRDA), a neurodegenerative disease caused by the decreased expression of mitochondrial protein frataxin. Nrf2, master regulator tissue redox balance, defective disease, driving cells to ferroptosis. Neuro-inflammation recently emerging as an additional pathological mechanism FRDA and has be understood order go deeper into pathogenesis disease. As functional cross talk between Nrf2 NF-kB pathways been previously reported, we wonder if inflammation may activated consequence deficiency. Thus, analyzed proteins involved antioxidant inflammatory responses fibroblasts patients with FRDA. We found significant activation TLR4/NF-kB/IL-1β axis patients, associated consistent increase enzymes thioredoxin 1 (TRX1) glutaredoxin (GLRX1), which are essential activate under oxidative stress conditions. Furthermore, investigated role 4-HNE, by-product lipid peroxidation, potential mediator ferroptosis

Язык: Английский

Insights into emerging mechanisms of ferroptosis: new regulators for cancer therapeutics DOI Creative Commons
Siyi Xu,

Shuangshuang Yin,

Lei Wang

и другие.

Cell Biology and Toxicology, Год журнала: 2025, Номер 41(1)

Опубликована: Март 25, 2025

Ferroptosis is an iron-dependent form of regulated cell death characterized by the accumulation lipid peroxides, which has been implicated in pathogenesis various diseases, and therapeutic agents targeting ferroptosis are emerging as promising tools for cancer treatment. Current research reveals that ferroptosis-targeted therapies can effectively inhibit tumor progression or delay development. Notably, natural product-derived compounds-such artemisinin, baicalin, puerarin, quercetin, kaempferol, apigenin-have demonstrated ability to modulate ferroptosis, offering potential anti-cancer benefits. Mechanistically, exhibits negative glutathione peroxidase 4 (GPX4) regulation demonstrates a positive correlation with plasma membrane polyunsaturated fatty acid (PUFA) abundance. Moreover, labile iron pool (LIP) serves redox engine ferroptosis. This review systematically analyzes hallmarks, signaling pathways, molecular mechanisms focus on how small molecules regulate this process. It further evaluates their inducers inhibitors anti-tumor therapy, providing foundation future clinical translation.

Язык: Английский

Процитировано

0
Redox homeostasis and inflammation in fibroblasts of patients with Friedreich Ataxia: a possible cross talk DOI Creative Commons
Andrea Quatrana, Sara Petrillo,

Caterina Torda

и другие.

Frontiers in Molecular Neuroscience, Год журнала: 2025, Номер 18

Опубликована: Апрель 16, 2025

Redox homeostasis is impaired in Friedreich’s Ataxia (FRDA), a neurodegenerative disease caused by the decreased expression of mitochondrial protein frataxin. Nrf2, master regulator tissue redox balance, defective disease, driving cells to ferroptosis. Neuro-inflammation recently emerging as an additional pathological mechanism FRDA and has be understood order go deeper into pathogenesis disease. As functional cross talk between Nrf2 NF-kB pathways been previously reported, we wonder if inflammation may activated consequence deficiency. Thus, analyzed proteins involved antioxidant inflammatory responses fibroblasts patients with FRDA. We found significant activation TLR4/NF-kB/IL-1β axis patients, associated consistent increase enzymes thioredoxin 1 (TRX1) glutaredoxin (GLRX1), which are essential activate under oxidative stress conditions. Furthermore, investigated role 4-HNE, by-product lipid peroxidation, potential mediator ferroptosis

Язык: Английский

Процитировано

0