A5078444427- Neuroscience and Neuropharmacology Research
- Ferroptosis and cancer prognosis
- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Mitochondrial Function and Pathology
- interferon and immune responses
- Photoreceptor and optogenetics research
- Nicotinic Acetylcholine Receptors Study
- Inflammasome and immune disorders
- Trace Elements in Health
- Retinal Diseases and Treatments
- Drug Transport and Resistance Mechanisms
- Cholesterol and Lipid Metabolism
- Ion channel regulation and function
- Glaucoma and retinal disorders
- Retinal Development and Disorders
University of Chile
2021-2025
Ferroptosis, a newly described form of regulated cell death, is characterized by the iron-dependent accumulation lipid peroxides, glutathione depletion, mitochondrial alterations, and enhanced lipoxygenase activity. Inhibition peroxidase 4 (GPX4), key intracellular antioxidant regulator, promotes ferroptosis in different types. Scant information available on GPX4-induced hippocampal neurons. Moreover, role calcium (Ca2+) signaling remains elusive. Here, we report that RSL3, selective...
Ferroptosis is an iron-dependent cell death pathway that involves the depletion of intracellular glutathione (GSH) levels and iron-mediated lipid peroxidation. experimentally caused by inhibition cystine/glutamate antiporter xCT, which depletes cells GSH, or peroxidase 4 (GPx4), a key regulator The events occur between GPx4 execution ferroptotic are currently matter active research. Previous work has shown calcium release from endoplasmic reticulum (ER) mediated ryanodine receptor (RyR)...
Ferroptosis is an iron-dependent cell death pathway that involves depletion of intracellular glutathione (GSH) levels and iron-mediated lipid peroxidation. experimentally caused by inhibition the cystine/glutamate antiporter xCT, which depletes cells GSH, or Glutathione peroxidase 4 (GPx4), a key regulator The events occur between GPx4 execution ferroptotic are currently matter active research. Previous work has shown calcium release from endoplasmic reticulum (ER) mediated ryanodine...
Hippocampal neuronal activity generates dendritic and somatic Ca2+ signals, which, depending on stimulus intensity, rapidly propagate to the nucleus induce expression of transcription factors genes with crucial roles in cognitive functions. Soluble amyloid-beta oligomers (AβOs), main synaptotoxins engaged pathogenesis Alzheimer's disease, generate aberrant signals primary hippocampal neurons, increase their oxidative tone disrupt structural plasticity. Here, we explored effects sub-lethal...
Hippocampal neuronal activity generates dendritic and somatic Ca2+ signals, which depending on stimulus intensity, rapidly propagate to the nucleus induce expression of transcription factors genes with crucial roles in cognitive functions. Soluble Amyloid-beta Oligomers (AβOs), main synaptotoxins engaged pathogenesis Alzheimer's disease, generate aberrant signals primary hippocampal neurons, increase their oxidative tone disrupt structural plasticity. Here, we explored effects...