Necroptosis

Croker, Ben A.; Rickard, James A; Shlomovitz, Inbar; Al-Obeidi, Arshed; D’Cruz, Akshay A.; Gerlic, Motti

doi:10.1002/9781119432463.ch6

Cited by 2 publications

(3 citation statements)

References 138 publications

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“…In addition to mechanical cell destruction, necroptosis is the main cell death pathway at the acute phase of traumatic brain injury (TBI), intracerebral or subarachnoid hemorrhage (SAH), and ischemic stroke (IS) [ 9 , 20 , 32 ]. Necroptosis is a morphologically lytic form of cell death implicating the receptor-interacting protein kinase 1 and 3 (RIPK1-RIPK3) and the mixed-lineage kinase domain-like pseudokinase (MLKL) pathway, resulting in the release of the contents of the cell into the extracellular space [ 33 ] ( Figure 1 A). The subsequent release of DAMPs peaks around 24 h after the primary insult and decreases thereafter over several days [ 4 , 12 , 20 , 34 , 35 , 36 , 37 , 38 ].…”

Section: Acute Lesion Progression Pathophysiologymentioning

confidence: 99%

“…The progression of secondary lesions follows different pathways. The ligation of TNF to the TNF receptor 1 (TNFR1) expressed by neurons will induce both necroptosis (via RIP1-3 and MLKL) and apoptosis (via caspase 3 and 8) [ 9 , 33 ]. Moreover, the pro-inflammatory cocktail can also activate astrocytes with a destructive phenotype (termed A1) leading to neuronal death and fewer synapses [ 7 ] ( Figure 1 C).…”

Section: Acute Lesion Progression Pathophysiologymentioning

confidence: 99%

“…Its role after acute brain injury remains controversial [ 119 , 120 ], and the safety and efficacy of a strategy resulting in autophagy down-regulation remains to be evaluated. Another cell death pathway involves the release of TNF that binds the TNFR1 leading to both necroptosis and apoptosis [ 9 , 33 ]. The intracellular recruitment of RIPK1 by TNFR1 starts a cascade that leads to cell death.…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

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DAMPs and RAGE Pathophysiology at the Acute Phase of Brain Injury: An Overview

Balança¹,

Desmurs²,

Grelier³

et al. 2021

IJMS

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Early or primary injury due to brain aggression, such as mechanical trauma, hemorrhage or is-chemia, triggers the release of damage-associated molecular patterns (DAMPs) in the extracellular space. Some DAMPs, such as S100B, participate in the regulation of cell growth and survival but may also trigger cellular damage as their concentration increases in the extracellular space. When DAMPs bind to pattern-recognition receptors, such as the receptor of advanced glycation end-products (RAGE), they lead to non-infectious inflammation that will contribute to necrotic cell clearance but may also worsen brain injury. In this narrative review, we describe the role and ki-netics of DAMPs and RAGE at the acute phase of brain injury. We searched the MEDLINE database for “DAMPs” or “RAGE” or “S100B” and “traumatic brain injury” or “subarachnoid hemorrhage” or “stroke”. We selected original articles reporting data on acute brain injury pathophysiology, from which we describe DAMPs release and clearance upon acute brain injury, and the implication of RAGE in the development of brain injury. We will also discuss the clinical strategies that emerge from this overview in terms of biomarkers and therapeutic perspectives

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Section: Acute Lesion Progression Pathophysiologymentioning

confidence: 99%

Section: Acute Lesion Progression Pathophysiologymentioning

confidence: 99%

Section: Therapeutic Perspectivesmentioning

confidence: 99%

See 1 more Smart Citation

DAMPs and RAGE Pathophysiology at the Acute Phase of Brain Injury: An Overview

Balança¹,

Desmurs²,

Grelier³

et al. 2021

IJMS

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Ultrastructural Analysis of Thalamus Damages in a Mouse Model of Osmotic-Induced Demyelination

et al. 2019

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A murine model used to investigate the osmotic demyelination syndrome (ODS) demonstrated ultrastructural damages in thalamus nuclei. Following chronic hyponatremia, significant myelinolysis was merely detected 48 h after the rapid reinstatement of normonatremia (ODS 48 h). In ODS samples, oligodendrocytes and astrocytes revealed injurious changes associated with a few cell deaths while both cell types seemed to endure a sort of survival strategy: (a) ODS 12 h oligodendrocytes displayed nucleoplasm with huge heterochromatic compaction, mitochondria hypertrophy, and most reclaimed an active NN cell aspect at ODS 48 h. (b) Astrocytes responded to the osmotic stress by overall cell shrinkage with clasmatodendrosis, these changes accompanied nucleus wrinkling, compacted and segregated nucleolus, destabilization of astrocyte-oligodendrocyte junctions, loss of typical GFAP filaments, and detection of round to oblong woolly, proteinaceous aggregates. ODS 48 h astrocytes regained an active nucleus aspect, without restituting GFAP filaments and still contained cytoplasmic proteinaceous deposits. (c) Sustaining minor shrinking defects at ODS 12 h, neurons showed slight axonal injury. At ODS 48 h, neuron cell bodies emerged again with deeply indented nucleus and, owing nucleolus translational activation, huge amounts of polysomes along with secretory-like activities. (d) In ODS, activated microglial cells got stuffed with huge lysosome bodies out of captures cell damages, leaving voids in interfascicular and sub-vascular neuropil. Following chronic hyponatremia, the murine thalamus restoration showed macroglial cells acutely turned off transcriptional and translational activities during ODS and progressively recovered activities, unless severely damaged cells underwent cell death, leading to neuropil disruption and demyelination.

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Necroptosis

Cited by 2 publications

References 138 publications

DAMPs and RAGE Pathophysiology at the Acute Phase of Brain Injury: An Overview

DAMPs and RAGE Pathophysiology at the Acute Phase of Brain Injury: An Overview

Ultrastructural Analysis of Thalamus Damages in a Mouse Model of Osmotic-Induced Demyelination

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