Journal ArticleDOI
Molecular targets in cerebral ischemia for developing novel therapeutics.
TLDR
The current status on the molecular mechanisms of stroke pathophysiology is covered with an endeavour to identify potential molecular targets such as targeting postsynaptic density-95 (PSD-95)/N-methyl-d-aspartate (NMDA) receptor interaction, certain key proteins involved in oxidative stress, CaMKs and MAPKs (ERK, p38 and JNK) signalling, inflammation and cell death pathways.About:
This article is published in Brain Research Reviews.The article was published on 2007-04-01. It has received 667 citations till now. The article focuses on the topics: Necroptosis & p38 mitogen-activated protein kinases.read more
Citations
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Mammalian caspases: structure ,a ctivation ,s ubstrates, and functions during apoptosis
TL;DR: Caspases, a family of cysteine-dependent aspartate-directed proteases, are prominent among the death proteases as discussed by the authors, and they play critical roles in initiation and execution of this process.
Journal ArticleDOI
Neuroprotection for ischemic stroke: past, present and future.
TL;DR: A close survey of the most extensively evaluated neuroprotective agents and classes is presented and considers both the strengths and weakness of the pre-clinical evidence as well as the results and shortcomings of the clinical trials themselves.
Journal ArticleDOI
Mitochondrial dysfunction and oxidative stress in metabolic disorders — A step towards mitochondria based therapeutic strategies
TL;DR: The purpose of the article is to highlight the recent progress on the mitochondrial role in metabolic syndromes and also summarize the progress of mitochondria-targeted molecules as therapeutic targets to treat metabolic Syndromes.
Journal ArticleDOI
Mitochondria, oxidative metabolism and cell death in stroke
Neil R. Sims,Hakan Muyderman +1 more
TL;DR: Pharmacological interventions and genetic modifications in rodent models strongly implicate caspase-dependent and caspases-independent apoptosis and the mitochondrial permeability transition as important contributors to tissue damage, particularly when induced by short periods of temporary focal ischemia.
Journal ArticleDOI
Pathophysiology, treatment, and animal and cellular models of human ischemic stroke
Trent M. Woodruff,John Thundyil,Sung-Chun Tang,Christopher G. Sobey,Stephen M. Taylor,Thiruma V. Arumugam +5 more
TL;DR: This review explores the etiology and pathogenesis of ischemic stroke, and provides a general model of such, and explores new and emerging approaches for the prevention and treatment of stroke.
References
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Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.
TL;DR: Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.
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Apparent hydroxyl radical production by peroxynitrite: implications for endothelial injury from nitric oxide and superoxide.
TL;DR: It is proposed that superoxide dismutase may protect vascular tissue stimulated to produce superoxide and NO under pathological conditions by preventing the formation of peroxynitrite.
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Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
TL;DR: Overexpressed Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3-dependent cell line and counters the death repressor activity of B cl-2, suggesting a model in which the ratio of Bcl-2 to Bax determines survival or death following an apoptotic stimulus.
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Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis
TL;DR: The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells.