We are analyzing https://link.springer.com/article/10.1007/s12975-013-0283-0.

Title:
Mitochondrial Dysfunction Induced by Nuclear Poly(ADP-Ribose) Polymerase-1: a Treatable Cause of Cell Death in Stroke | Translational Stroke Research
Description:
Many drugs targeting excitotoxic cell death have demonstrated robust neuroprotective effects in animal models of cerebral ischemia. However, these neuroprotective effects have almost universally required drug administration at relatively short time intervals after ischemia onset. This finding has translated to clinical trial results; interventions targeting excitotoxicity have had no demonstrable efficacy when initiated hours after ischemia onset, but beneficial effects have been reported with more rapid initiation. Consequently, there continues to be a need for interventions with efficacy at later time points after ischemia. Here, we focus on mitochondrial dysfunction as both a relatively late event in ischemic neuronal death and a recognized cause of delayed neuronal death. Activation of poly(ADP-ribose) polymerase-1 (PARP-1) is a primary cause of mitochondrial depolarization and subsequent mitochondria-triggered cell death in ischemia reperfusion. PARP-1 consumes cytosolic NAD+, thereby blocking both glycolytic ATP production and delivery of glucose carbon to mitochondria for oxidative metabolism. However, ketone bodies such as pyruvate, beta- and gamma-hydroxybutyrate, and 1,4-butanediol can fuel mitochondrial metabolism in cells with depleted cytosolic NAD+ as long as the mitochondria remain functional. Ketone bodies have repeatedly been shown to be highly effective in preventing cell death in animal models of ischemia, but a rigorous study of the time window of opportunity for this approach remains to be performed.
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Keywords {🔍}

pubmed, google, scholar, article, cas, death, cell, cerebral, brain, ischemia, polyadpribose, mitochondrial, swanson, stroke, central, polymerase, neuronal, focal, pyruvate, neurosci, rat, ischemic, metab, transient, apoptosis, cereb, blood, flow, res, nad, mitochondria, injury, wang, chen, activation, glutamate, damage, pharmacol, kim, protection, research, models, nmda, protects, dis, sci, permeability, transition, lee, privacy,

Topics {✒️}

n-methyl-d-aspartate receptor antagonist ascorbate/menadione-induced oxidative stress n-methyl-d-aspartate receptors n-methyl-d-aspartate antagonists month download article/chapter n-methyl-d-aspartate mitochondrial apoptosis-inducing factor ischemia-induced hippocampal neurodegeneration cerebral ischemia-induced neurodegeneration hypoxic-ischemic brain injury polymer-induced cell death mitochondrial dysfunction induced polymerase-1-mediated cell death polymerase-1-mediated neuronal death full article pdf mitochondrial permeability transition yu sw apoptotic neuronal death ceramide-induced apoptosis ischemic neuronal death privacy choices/manage cookies alano cc fuel glutamate uptake excitotoxic cell death cerebral ischemic injury giffard rg preventing cell death cell death differ cell death caused anti-cell death excitotoxic neuronal death brain dysfunctions induced focal cerebral damage delayed neuronal death hypoglycemic neuronal death necrotic cell death ischemic damage caused ischemic brain injury california san francisco ischemic brain damage central executioner related subjects andrabi sa cellular response focal cerebral ischemia cell death dis simon rp article baxter selective cell loss nicholls dg

Questions {❓}

Apoptosis after experimental stroke: fact or fashion?
The mitochondrial permeability transition pore: a mystery solved?

Schema {🗺️}

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         description:Many drugs targeting excitotoxic cell death have demonstrated robust neuroprotective effects in animal models of cerebral ischemia. However, these neuroprotective effects have almost universally required drug administration at relatively short time intervals after ischemia onset. This finding has translated to clinical trial results; interventions targeting excitotoxicity have had no demonstrable efficacy when initiated hours after ischemia onset, but beneficial effects have been reported with more rapid initiation. Consequently, there continues to be a need for interventions with efficacy at later time points after ischemia. Here, we focus on mitochondrial dysfunction as both a relatively late event in ischemic neuronal death and a recognized cause of delayed neuronal death. Activation of poly(ADP-ribose) polymerase-1 (PARP-1) is a primary cause of mitochondrial depolarization and subsequent mitochondria-triggered cell death in ischemia reperfusion. PARP-1 consumes cytosolic NAD+, thereby blocking both glycolytic ATP production and delivery of glucose carbon to mitochondria for oxidative metabolism. However, ketone bodies such as pyruvate, beta- and gamma-hydroxybutyrate, and 1,4-butanediol can fuel mitochondrial metabolism in cells with depleted cytosolic NAD+ as long as the mitochondria remain functional. Ketone bodies have repeatedly been shown to be highly effective in preventing cell death in animal models of ischemia, but a rigorous study of the time window of opportunity for this approach remains to be performed.
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      description:Many drugs targeting excitotoxic cell death have demonstrated robust neuroprotective effects in animal models of cerebral ischemia. However, these neuroprotective effects have almost universally required drug administration at relatively short time intervals after ischemia onset. This finding has translated to clinical trial results; interventions targeting excitotoxicity have had no demonstrable efficacy when initiated hours after ischemia onset, but beneficial effects have been reported with more rapid initiation. Consequently, there continues to be a need for interventions with efficacy at later time points after ischemia. Here, we focus on mitochondrial dysfunction as both a relatively late event in ischemic neuronal death and a recognized cause of delayed neuronal death. Activation of poly(ADP-ribose) polymerase-1 (PARP-1) is a primary cause of mitochondrial depolarization and subsequent mitochondria-triggered cell death in ischemia reperfusion. PARP-1 consumes cytosolic NAD+, thereby blocking both glycolytic ATP production and delivery of glucose carbon to mitochondria for oxidative metabolism. However, ketone bodies such as pyruvate, beta- and gamma-hydroxybutyrate, and 1,4-butanediol can fuel mitochondrial metabolism in cells with depleted cytosolic NAD+ as long as the mitochondria remain functional. Ketone bodies have repeatedly been shown to be highly effective in preventing cell death in animal models of ischemia, but a rigorous study of the time window of opportunity for this approach remains to be performed.
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