2012
DOI: 10.1111/j.1747-4949.2012.00839.x
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Pathophysiologic Cascades in Ischemic Stroke

Abstract: Many advances have been achieved in terms of understanding the molecular and cellular mechanisms of ischemic stroke. But thus far, clinically effective neuroprotectants remain elusive. In this minireview, we summarize the basics of ischemic cascades after stroke, covering neuronal death mechanisms, white matter pathophysiology, and inflammation with an emphasis on microglia. Translating promising mechanistic knowledge into clinically meaningful stroke drugs is very challenging. An integrative approach that enc… Show more

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Cited by 326 publications
(233 citation statements)
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“…14,15 Considerable attention has been paid to the putative role of PON1 activity and its polymorphisms as a risk factor for ischemic stroke, one of the main neurological diseases associated with atherosclerosis. [16][17][18][19] Several comprehensive reviews and meta-analysis including studies up to 2011 are available. 16,20,21 Beyond stroke, oxidative stress plays a key role in many neurodegenerative diseases, although the precise pathogenic links are yet to be elucidated.…”
Section: Introductionmentioning
confidence: 99%
“…14,15 Considerable attention has been paid to the putative role of PON1 activity and its polymorphisms as a risk factor for ischemic stroke, one of the main neurological diseases associated with atherosclerosis. [16][17][18][19] Several comprehensive reviews and meta-analysis including studies up to 2011 are available. 16,20,21 Beyond stroke, oxidative stress plays a key role in many neurodegenerative diseases, although the precise pathogenic links are yet to be elucidated.…”
Section: Introductionmentioning
confidence: 99%
“…O AVCI também é importante fator de morbidade, sendo responsável por várias sequelas como: distúrbios motores, distúrbios do sono e depressão 31 . A fisiopatogênese do AVCI envolve a redução da concentração de adenosina trifosfato (ATP), devido a uma queda na sua produção, pela isquemia, que, por sua vez, também leva a uma acidose lática e desequilíbrio na homeostase iônica dos neurônios 32 .…”
unclassified
“…It is thought that after ischemia, cytoplasmic Ca 2+ levels rise that can trigger overproduction of free radicals, dysfunction of mitochondria, cell membrane disruption and DNA fragmentation, which acting synergistically cause neuron death. After cerebral ischemia and particularly after reperfusion, robust oxidants are generated including superoxide and hydroxyl radicals, which overwhelm endogenous scavenging mechanisms and are directly involved in the damage to cellular macromolecules 12,13 .…”
Section: Discussionmentioning
confidence: 99%