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Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia.
Antioxid Redox Signal. 2003 Oct; 5(5):597-607.AR

Abstract

Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible targets of this redox signaling include mitochondria, death membrane receptors, and DNA repair enzymes. Genetic manipulation of intrinsic antioxidants and the factors in the signaling pathways has provided substantial progress in understanding the mechanisms in cell death signaling pathways and involvement of oxygen radicals in ischemic brain injury. Future studies of these pathways may provide novel therapeutic strategies in clinical stroke.

Authors+Show Affiliations

Department of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, CA 94305, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

Language

eng

PubMed ID

14580316

Citation

Sugawara, Taku, and Pak H. Chan. "Reactive Oxygen Radicals and Pathogenesis of Neuronal Death After Cerebral Ischemia." Antioxidants & Redox Signaling, vol. 5, no. 5, 2003, pp. 597-607.
Sugawara T, Chan PH. Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia. Antioxid Redox Signal. 2003;5(5):597-607.
Sugawara, T., & Chan, P. H. (2003). Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia. Antioxidants & Redox Signaling, 5(5), 597-607.
Sugawara T, Chan PH. Reactive Oxygen Radicals and Pathogenesis of Neuronal Death After Cerebral Ischemia. Antioxid Redox Signal. 2003;5(5):597-607. PubMed PMID: 14580316.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reactive oxygen radicals and pathogenesis of neuronal death after cerebral ischemia. AU - Sugawara,Taku, AU - Chan,Pak H, PY - 2003/10/29/pubmed PY - 2004/6/16/medline PY - 2003/10/29/entrez SP - 597 EP - 607 JF - Antioxidants & redox signaling JO - Antioxid Redox Signal VL - 5 IS - 5 N2 - Reactive oxygen species have been implicated in brain injury after cerebral ischemia. These oxidants can damage proteins, lipids, and DNA, and lead to cell injury and necrosis. Oxidants are also initiators in intracellular cell death signaling pathways that may lead to apoptosis. The possible targets of this redox signaling include mitochondria, death membrane receptors, and DNA repair enzymes. Genetic manipulation of intrinsic antioxidants and the factors in the signaling pathways has provided substantial progress in understanding the mechanisms in cell death signaling pathways and involvement of oxygen radicals in ischemic brain injury. Future studies of these pathways may provide novel therapeutic strategies in clinical stroke. SN - 1523-0864 UR - https://www.unboundmedicine.com/medline/citation/14580316/Reactive_oxygen_radicals_and_pathogenesis_of_neuronal_death_after_cerebral_ischemia_ L2 - https://www.liebertpub.com/doi/10.1089/152308603770310266?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -