Mitophagy is a process whereby cells selectively remove mitochondria through the mechanism of autophagy, which plays an important role in maintaining cellular homeostasis. In order to explore the effect of mitophagy genes on the antioxidant activities of , mutants with deletion or overexpression of mitophagy genes , and were constructed respectively. The results indicated that overexpression of and genes significantly reduced the intracellular reactive oxygen species (ROS) content upon HO stress for 6 h, which were 61.23% and 46.35% of the initial state, respectively. Notable, overexpression of and genes significantly increased the mitochondrial membrane potential (MMP) and ATP content, which were helpful to improve the antioxidant activities of the strains. On the other hand, deletion of , and caused mitochondrial damage and significantly decreased cell vitality, and caused the imbalance of intracellular ROS. The intracellular ROS content significantly increased to 174.27%, 128.68%, 200.92% of the initial state, respectively, upon HO stress for 6 h. The results showed that , and might be potential targets for regulating the antioxidant properties of yeast, providing a new clue for further research.
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http://dx.doi.org/10.13345/j.cjb.220860 | DOI Listing |
J Gastroenterol Hepatol
January 2025
Department of Pharmacology, Hepatology and Molecular Medicine Lab, Saveetha Dental College and Hospitals, Saveetha Institute of Medical and Technical Sciences (SIMATS), Chennai, Tamil Nadu, India.
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View Article and Find Full Text PDFiScience
January 2025
Department of Microbiology and Immunology, Penn State College of Medicine, Hershey, PA 17033, USA.
ZFAND6 is a zinc finger protein that interacts with TNF receptor-associated factor 2 (TRAF2) and polyubiquitin chains and has been linked to tumor necrosis factor (TNF) signaling. Here, we report a previously undescribed function of ZFAND6 in maintaining mitochondrial homeostasis by promoting mitophagy. Deletion of ZFAND6 in bone marrow-derived macrophages (BMDMs) upregulates reactive oxygen species (ROS) and the accumulation of damaged mitochondria due to impaired mitophagy.
View Article and Find Full Text PDFNat Rev Drug Discov
January 2025
Mission Therapeutics Ltd, Babraham Research Campus, Cambridge, UK.
Mitochondrial dysfunction is a hallmark of idiopathic neurodegenerative diseases, including Parkinson disease, amyotrophic lateral sclerosis, Alzheimer disease and Huntington disease. Familial forms of Parkinson disease and amyotrophic lateral sclerosis are often characterized by mutations in genes associated with mitophagy deficits. Therefore, enhancing the mitophagy pathway may represent a novel therapeutic approach to targeting an underlying pathogenic cause of neurodegenerative diseases, with the potential to deliver neuroprotection and disease modification, which is an important unmet need.
View Article and Find Full Text PDFSkelet Muscle
January 2025
Department of Anesthesia and Critical Care, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Background: Duchenne muscular dystrophy (DMD) is a prevalent, fatal degenerative muscle disease with no effective treatments. Mdx mouse model of DMD exhibits impaired muscle performance, oxidative stress, and dysfunctional autophagy. Although antioxidant treatments may improve the mdx phenotype, the precise molecular mechanisms remain unclear.
View Article and Find Full Text PDFCancer Cell Int
January 2025
Department of Blood Transfusion, China-Japan, Union Hospital of Jilin University, Changchun, 130033, P.R. China.
Deapioplatycodin D (DPD) is a triterpenoid saponin natural compound isolated from the Chinese herb Platycodon grandiflorum that has antiviral and antitumor properties. This study aimed to investigate the effects of DPD on glioblastoma (GBM) cells and to determine its intrinsic mechanism of action. Using a CCK8 assay, it was found that DPD significantly inhibited the growth of GBM cells.
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