Role of mitochondria in apoptotic and necroptotic cell death in the developing brain
| العنوان: | Role of mitochondria in apoptotic and necroptotic cell death in the developing brain |
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| المؤلفون: | Claire Thornton, Henrik Hagberg |
| المصدر: | Clinica Chimica Acta; International Journal of Clinical Chemistry |
| بيانات النشر: | Elsevier BV, 2015. |
| سنة النشر: | 2015 |
| مصطلحات موضوعية: | TWEAK, tumor necrosis factor (ligand) superfamily, member 12, Clinical Biochemistry, Apoptosis, Mitochondrion, Biochemistry, Calcium in biology, Perinatal brain injury, Apaf-1, apoptotic protease activating factor 1, 0302 clinical medicine, MOMP, mitochondrial outer membrane permeabilization, MLKL, mixed lineage kinase domain-like protein, Calcium signaling, Neurons, TNF, tumor necrosis factor, 0303 health sciences, Cell Death, General Medicine, Mitochondria, 3. Good health, Cell biology, Necroptosis, Hypoxia-Ischemia, Brain, MP, mitochondrial permeabilization, LPS, lipopolysaccharide, TRIF, TIR-domain-containing adapter-inducing interferon-β, Intracellular, TLR, Toll-like receptor, Programmed cell death, AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, cyt c, cytochrome c, ATP, adenosine triphosphate, TRADD, tumor necrosis factor receptor type 1-associated DEATH domain, ENDO, endonuclease, RIP, receptor-interacting serine/threonine-protein kinase 1, Biology, Neuroprotection, Article, Drp-1, dynamin-related protein 1, Necrosis, 03 medical and health sciences, ROS, reactive oxygen species, Cy, cyclophilin, Animals, Humans, 030304 developmental biology, Biochemistry, medical, NO, nitric oxide, NMDA, N-methyl-D-aspartate, TRAIL, TNF-related apoptosis-inducing ligand, CAD, caspase-activation DNase, Biochemistry (medical), Hypoxia–ischemia, AIF, apoptosis-inducing factor, HI, hypoxia–ischemia, 030217 neurology & neurosurgery |
| الوصف: | Hypoxic–ischemic encephalopathy induces secondary brain injury characterized by delayed energy failure. Currently, therapeutic hypothermia is the sole treatment available after severe intrapartum asphyxia in babies and acts to attenuate secondary loss of high energy phosphates improving both short- and long-term outcome. In order to develop the next generation of neuroprotective therapies, we urgently need to understand the underlying molecular mechanisms leading to cell death. Hypoxia–ischemia creates a toxic intracellular environment including accumulation of reactive oxygen/nitrosative species and intracellular calcium after the insult, inducing mitochondrial impairment. More specifically mitochondrial respiration is suppressed and calcium signaling is dysregulated. At a certain threshold, Bax-dependent mitochondrial permeabilization will occur leading to activation of caspase-dependent and apoptosis-inducing factor-dependent apoptotic cell death. In addition, hypoxia–ischemia induces inflammation, which leads to the release of TNF-α, TRAIL, TWEAK, FasL and Toll-like receptor agonists that will activate death receptors on neurons and oligodendroglia. Death receptors trigger apoptotic death via caspase-8 and necroptotic cell death through formation of the necrosome (composed of RIP1, RIP3 and MLKL), both of which converge at the mitochondria. Highlights • Hypoxic-ischemic encephalopathy induces secondary brain injury characterized by delayed energy failure and excitotoxicity. • Hypoxia-ischemia triggers accumulation of reactive oxygen species andintracellular calcium, which induces mitochondrial dysfunction. • Mitochondrial impairment can cause Bax-dependent mitochondrial permeabilization, which triggers release of pro-apoptotic proteins and cell death. • During the recovery phase, Inflammation is produced leading to death receptor activation and induction of necroptosis. |
| تدمد: | 0009-8981 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::912061e0597cce571c96e765b5ed8dcfTest https://doi.org/10.1016/j.cca.2015.01.026Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....912061e0597cce571c96e765b5ed8dcf |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 00098981 |
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