Apoptotic mechanisms after cerebral ischemia

Broughton, Brad R. S., Reutens, David C. and Sobey, Christopher G. (2009) Apoptotic mechanisms after cerebral ischemia. Stroke, 40 5: e331-e339. doi:10.1161/STROKEAHA.108.531632

Author Broughton, Brad R. S.
Reutens, David C.
Sobey, Christopher G.
Title Apoptotic mechanisms after cerebral ischemia
Journal name Stroke   Check publisher's open access policy
ISSN 0039-2499
Publication date 2009-05-01
Year available 2009
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1161/STROKEAHA.108.531632
Volume 40
Issue 5
Start page e331
End page e339
Total pages 9
Editor Vladimir Hachinski
Place of publication Philadelphia, PA, United States
Publisher American Heart Association
Collection year 2010
Language eng
Subject 11 Medical and Health Sciences
Formatted abstract
Background and Purpose—
Traditionally, cell death after cerebral ischemia was considered to be exclusively necrotic in nature, but research over the past decade has revealed that after a stroke, many neurons in the ischemic penumbra will undergo apoptosis.

Summary of Review—

This brief review provides a general overview and update of various signaling pathways in the development of apoptosis in ischemic lesions. Cerebral ischemia triggers two general pathways of apoptosis: the intrinsic pathway, originating from mitochondrial release of cytochrome c and associated stimulation of caspase-3; and the extrinsic pathway, originating from the activation of cell surface death receptors, resulting in the stimulation of caspase-8. Although many of the key apoptotic proteins have been identified, our understanding of the complex underlying mechanisms remains poor and hence treatment of stroke patients by manipulating apoptotic pathways remains a daunting task. However, recent advances in the field have helped broaden our knowledge of apoptosis after cerebral ischemia. Further to the simplistic concept that stroke-induced apoptosis occurs predominantly in neurons and is caspase-dependent, accumulating evidence now indicates that apoptosis is prevalent in nonneuronal cells and that caspase-independent mechanisms also play a key role.

Although the ischemic penumbra is under threat of infarction, it is potentially salvageable and thus represents an opportunity for therapeutic intervention.
Keyword Stroke
Cytochrome C
Fas receptor
Neuronal Cell-death
Subsequent DNA Fragment
Oxygen Glucose Deprivation
Mitochondrial Cytochrome-C
Transient Focal Iscehmia
Transgenic Mice Protects
Artery Occlusion
Brain injury
Poly(adp-ribose) Polymerase
Nuclear Translocation
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Queensland Brain Institute Publications
ERA 2012 Admin Only
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 363 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 442 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Fri, 13 Nov 2009, 08:01:55 EST