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Prognostic significance and therapeutic potential of guanosine triphosphate cyclohydrolase 1 in esophageal squamous cell carcinoma: clinical implications of ferroptosis and lipid peroxidation regulation.
Front Oncol
December 2024
Department of Human Pathology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
Background: Esophageal cancer, particularly esophageal squamous cell carcinoma (ESCC), is a leading cause of cancer-related death and has a poor prognosis. Despite the advancements in multidisciplinary therapies, resistance to conventional treatments warrants the development of novel therapeutic strategies. Ferroptosis, a form of cell death dependent on intracellular iron, has emerged as a potential mechanism for targeting cancer cells resistant to apoptosis.
View Article and Find Full Text PDFCross-species RNAi therapy via AAV delivery alleviates neuropathic pain by targeting GCH1.
Neurotherapeutics
December 2024
Department of Neurosurgery, Yonsei University College of Medicine, Seoul, Republic of Korea; Department of Neurosurgery, Brain Research institute, Yonsei University College of Medicine, Seoul, Republic of Korea. Electronic address:
Tetrahydrobiopterin (BH4) expression is normally strictly controlled; however, its intracellular levels increase considerably following nerve damage. GTP cyclohydrolase I (GCH1) plays a crucial role in regulating BH4 concentration, with an upregulation observed in the dorsal root ganglion in cases of neuropathic pain. In this study, we aimed to develop and evaluate the clinical potential of an RNA interference-based adeno-associated virus (AAV) targeting GCH1 across various species to decrease BH4 levels and, consequently, alleviate neuropathic pain symptoms.
View Article and Find Full Text PDFBroadening horizons: the multifaceted role of ferroptosis in breast cancer.
Front Immunol
December 2024
Department of Rheumatology, The First People's Hospital Changde City, Changde, Hunan, China.
Article Synopsis
- - Breast cancer is a major global health issue for women, often complicated by current treatments like chemotherapy and radiotherapy that can lead to drug resistance and poor outcomes due to mechanisms like anti-apoptosis.
- - Ferroptosis is a new form of cell death linked to factors such as iron overload and oxidative stress, which has been shown to hinder cancer cell growth and increase sensitivity to standard treatments.
- - The paper reviews the mechanisms and signaling pathways involved in ferroptosis related to breast cancer, highlighting the need for more research to better understand its regulatory factors and improve treatment strategies.
CTRP13 attenuates atherosclerosis by inhibiting endothelial cell ferroptosis via activating GCH1.
Int Immunopharmacol
December 2024
Harbin Medical University, Harbin 150001, PR China; Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, PR China; Key Laboratory of Myocardial Ischemia, Ministry of Education, Harbin 150001, PR China. Electronic address:
C1q/TNF-related protein 13 (CTRP13) is a secreted adipokine that has been shown to play an important role in a variety of cardiovascular diseases. However, the effect of CTRP13 on ferroptosis of endothelial cells and its underlying mechanism remain unclear. In the present study, we analyzed the effects of CTRP13 on endothelial dysfunction in high-lipid-induced ApoE mice and ox-LDL-induced mouse aortic endothelial cells (MAECs).
View Article and Find Full Text PDFA protective role for EFTUD2 in the brain.
Neuron
October 2024
Research Institute of the McGill University Health Centre at Glen Site, Montreal, QC H4A 3J1, Canada; Department of Human Genetics, McGill University, Montreal, QC H3A 0G1, Canada; Department of Anatomy and Cell Biology, McGill University, Montreal, QC H3A 2B2, Canada; Department of Pediatrics, McGill University, Montreal, QC H4A 3J1, Canada. Electronic address:
In this issue of Neuron, Yang et al. report MFDM-like phenotypes in mice with deletion of Eftud2 in their Purkinje cells (PCs), namely cerebellar atrophy alongside motor and social deficits, similar to phenotypes observed in MFDM patients. The absence of Eftud2 caused mis-splicing of Atf4, reduced Scd1 and Gch1, and promoted ferroptosis-regulated PC death.
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