In the liver, reactive oxygen species (ROS) are constantly released during cellular metabolic processes, and excess ROS production can cause redox stress. The redox stress is both beneficial for and harmful to the survival of cells since it modulates the cellular redox control system. The redox control system is a series of cellular responses that are responsible for maintaining a balanced oxidation-reduction status. Many cellular processes including growth, proliferation, and senescence are sensitively regulated by the redox control system. Imbalance of redox induces redox stress and damages DNA, proteins, and lipids in cells, and further contributes to the pathogenesis of severe diseases and disorders like cancer. However, the cellular redox control system also utilizes redox stress-responsive pathways and increases antioxidant enzymes to aid cell survival. Therefore, a deeper understanding of the connection between the redox control system and liver disease is likely to pave the way for the future development of new therapeutic strategies. This review will examine the redox control systems in liver with responsive regulating molecules, current knowledge of the redox control system and liver disease, and suggest potential therapeutic targets for liver diseases.
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http://dx.doi.org/10.1016/j.biopha.2022.113764 | DOI Listing |
Sci Rep
January 2025
Department of Biochemistry, College of Science, King Saud University, P.O.Box 2455, Riyadh, 11451, Saudi Arabia.
Nano-biochar considers a versatile and valuable sorbent to enhance plant productivity by improving soil environment and emerged as a novel solution for environmental remediation and sustainable agriculture in modern era. In this study, roles of foliar applied nanobiochar colloidal solution (NBS) on salt stressed tomato plants were investigated. For this purpose, NBS was applied (0%, 1% 3% and 5%) on two groups of plants (control 0 mM and salt stress 60 mM).
View Article and Find Full Text PDFCell Death Dis
January 2025
CECAD Cluster of Excellence, University of Cologne, Cologne, Germany.
Constitutive mitochondrial dynamics ensure quality control and metabolic fitness of cells, and their dysregulation has been implicated in various human diseases. The large GTPase Dynamin-related protein 1 (Drp1) is intimately involved in mediating constitutive mitochondrial fission and has been implicated in mitochondrial cell death pathways. During ferroptosis, a recently identified type of regulated necrosis driven by excessive lipid peroxidation, mitochondrial fragmentation has been observed.
View Article and Find Full Text PDFInt J Food Microbiol
January 2025
School of Life Science and Technology, Shandong Second Medical University, Weifang, Shandong, China. Electronic address:
Escherichia coli O157:H7 has caused many foodborne disease outbreaks and resulted in unimaginable economic losses. With the evolution of food consumption, people prefer natural preservatives. In this study, the natural agent harmane exhibited potential activity against E.
View Article and Find Full Text PDFInt Immunopharmacol
January 2025
Complex Carbohydrate Research Center, University of Georgia, Athens, GA, USA. Electronic address:
Global healthcare systems are under tremendous strain due to the increasing prevalence of neurodegenerative disorders. Growing data suggested that overconsumption of high-fat/high-carbohydrates diet (HFHCD) is associated with enhanced incidence of metabolic alterations, neurodegeneration, and cognitive dysfunction. Functional foods have gained prominence in curbing metabolic and neurological deficits.
View Article and Find Full Text PDFNutrients
January 2025
Department of Food & Nutrition, Kyung Hee University, Seoul 02447, Republic of Korea.
Background/objectives: The pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH) is closely associated with increased oxidative stress and lipid peroxidation. Coenzyme Q (CoQ) and selenium (Se) are well-established antioxidants with protective effects against oxidative damage. This study aimed to investigate the effects of CoQ and Se in ameliorating MASH induced by a methionine choline-deficient (MCD) diet in mice.
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