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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.

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Diabetic retinopathy, a microvascular complication of diabetes, is the leading cause of blindness in adults, but the molecular mechanism of its development remains unclear. Retinal mitochondrial DNA is damaged and hypermethylated, and mtDNA-encoded genes are downregulated. Expression of a long noncoding RNA (larger than 200 nucleotides, which does not translate into proteins), encoded by mtDNA, cytochrome B (Lnc), is also downregulated.

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Introduction: Advanced glycation end products (AGEs) play a critical role in the development of vascular diseases in diabetes. Although stem cell therapies often involve exposure to AGEs, the impact of this environment on extracellular vesicles (EVs) and endothelial cell metabolism remains unclear.

Methods: Human umbilical cord mesenchymal stem cells (MSCs) were treated with either 0 ng/ml or 100 ng/ml AGEs in a serum-free medium for 48 hours, after which MSC-EVs were isolated.

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Over the past few decades, ocean hypoxia has been increasing due to human activities. Hypoxic stress, characterized by a reduced level of dissolved oxygen, is an escalating threat to marine ecosystems, with potentially devastating effects on the viability of endangered species such as the tri-spine horseshoe crab Tachypleus tridentatus. Even though this species is remarkably resilient to low oxygen levels, persistent hypoxia can negatively impact its population's survivability.

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Sub-Chronic 30 mg/kg Iron Treatment Induces Spatial Cognition Impairment and Brain Oxidative Stress in Wistar Rats.

Biol Trace Elem Res

January 2025

Laboratory Functional Physiology and Bio-Resources Valorisation, Higher Institute of Biotechnology of Beja, University of Jendouba, Avenue Habib Bourguiba BP 382, 9000, Beja, Tunisia.

Iron overload has been shown to have deleterious effects in the brain through the formation of reactive oxygen species, which ultimately may contribute to neurodegenerative disorders. Accordingly, rodent studies have indicated that systemic administration of iron produces excess iron in the brain and results in behavioral and cognitive deficits. To what extent cognitive abilities are affected and which neurobiological mechanisms underlie those deficits remain to be more fully characterized.

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