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| http://dx.doi.org/10.4103/1673-5374.390975 | DOI Listing |
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Hyperoxia-activated Nrf2 regulates ferroptosis in intestinal epithelial cells and intervenes in inflammatory reaction through COX-2/PGE2/EP2 pathway.
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Department of Gastroenterology and Medical Research Center, Liaoning Key Laboratory of Research and Application of Animal Models for Environmental and Metabolic Diseases, ShengJing Hospital of China Medical University, SanHao Street No. 36, HePing District, Shenyang, 110000, Liaoning, China.
The lack of knowledge about the mechanism of hyperoxia-induced intestinal injury has attracted considerable attention, due to the potential for this condition to cause neonatal complications. This study aimed to explore the relationship between hyperoxia-induced oxidative damage and ferroptosis in intestinal tissue and investigate the mechanism by which hyperoxia regulates inflammation through ferroptosis. The study systematically evaluated the effects of hyperoxia on oxidative stress, mitochondrial damage, ferroptosis, and inflammation of intestinal epithelial cells both in vitro and in vivo.
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National Key Laboratory of Veterinary Public Health Security, College of Veterinary Medicine, China Agricultural University, Haidian, Beijing 100193, China. Electronic address:
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View Article and Find Full Text PDFFerroptosis, an iron-dependent form of programmed cell death driven by oxidative stress, plays a crucial role in the progression of Alzheimer's disease (AD). Aging diminishes antioxidant systems that maintain iron homeostasis, particularly affecting the glutathione peroxidase (GPX) system, leading to increased ferroptosis and exacerbated neurodegeneration and neuroinflammation in AD. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor regulating genes involved in antioxidant defense and ferroptosis.
View Article and Find Full Text PDFAcacetin Attenuates Cigarette Smoke Extract-Induced Human Bronchial Epithelial Cell Injury by Activating NRF2/SLC7A11/GPX4 Signaling to Inhibit Ferroptosis.
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Yangzhou Hospital Affiliated to Nanjing University of Chinese Medicine, Yangzhou, 225000, Jiangsu, China.
Chronic obstructive pulmonary disease (COPD) stands as a major contributor to mortality worldwide, with cigarette smoke being a primary causative factor. Acacetin has been reported to possess lung protective effects. However, the precise role and mechanism of Acacetin in COPD remains elusive.
View Article and Find Full Text PDFBackground: In Alzheimer's disease (AD), histone acetylation is disrupted, suggesting loss of transcriptional control. Moreover, converging evidence suggests an age- and AD-dependent loss of transcription controlled by all-trans-retinoic acid (ATRA), the bioactive metabolite of vitamin A (VA). Antioxidant depletion causes oxidative stress (OS).
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