Apoptosis and Acute Brain Ischemia in Ischemic Stroke
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Аутори
Radak, Đorđe J.Katsiki, Niki
Resanović, Ivana
Jovanović, Aleksandra
Sudar, Emina
Zafirović, Sonja
Mousa, Shaker A.
Isenović, Esma R.
Приказ (Објављена верзија)
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Приказ свих података о документуАпстракт
Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. ...These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.
Кључне речи:
Apoptosis / acute brain ischemia / stroke / caspase / death receptor / statinsИзвор:
Current Vascular Pharmacology, 2017, 15, 2, 115-122Финансирање / пројекти:
- Каротидна болест у Србији - патолошка динамика, превенција, дијагностика и иновативни терапијски поступци (RS-41002)
- Хормонска регулација експресије и активности азот оксид синтазе и натријум-калијумове пумпе у експерименталним моделима инсулинске резистенције, дијабетеса и кардиоваскуларних поремећаја (RS-173033)
DOI: 10.2174/1570161115666161104095522
ISSN: 1570-1611; 1875-6212
PubMed: 27823556
WoS: 000399590800004
Scopus: 2-s2.0-85011048703
Колекције
Институција/група
VinčaTY - JOUR AU - Radak, Đorđe J. AU - Katsiki, Niki AU - Resanović, Ivana AU - Jovanović, Aleksandra AU - Sudar, Emina AU - Zafirović, Sonja AU - Mousa, Shaker A. AU - Isenović, Esma R. PY - 2017 UR - https://vinar.vin.bg.ac.rs/handle/123456789/1521 AB - Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered. T2 - Current Vascular Pharmacology T1 - Apoptosis and Acute Brain Ischemia in Ischemic Stroke VL - 15 IS - 2 SP - 115 EP - 122 DO - 10.2174/1570161115666161104095522 ER -
@article{ author = "Radak, Đorđe J. and Katsiki, Niki and Resanović, Ivana and Jovanović, Aleksandra and Sudar, Emina and Zafirović, Sonja and Mousa, Shaker A. and Isenović, Esma R.", year = "2017", abstract = "Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.", journal = "Current Vascular Pharmacology", title = "Apoptosis and Acute Brain Ischemia in Ischemic Stroke", volume = "15", number = "2", pages = "115-122", doi = "10.2174/1570161115666161104095522" }
Radak, Đ. J., Katsiki, N., Resanović, I., Jovanović, A., Sudar, E., Zafirović, S., Mousa, S. A.,& Isenović, E. R.. (2017). Apoptosis and Acute Brain Ischemia in Ischemic Stroke. in Current Vascular Pharmacology, 15(2), 115-122. https://doi.org/10.2174/1570161115666161104095522
Radak ĐJ, Katsiki N, Resanović I, Jovanović A, Sudar E, Zafirović S, Mousa SA, Isenović ER. Apoptosis and Acute Brain Ischemia in Ischemic Stroke. in Current Vascular Pharmacology. 2017;15(2):115-122. doi:10.2174/1570161115666161104095522 .
Radak, Đorđe J., Katsiki, Niki, Resanović, Ivana, Jovanović, Aleksandra, Sudar, Emina, Zafirović, Sonja, Mousa, Shaker A., Isenović, Esma R., "Apoptosis and Acute Brain Ischemia in Ischemic Stroke" in Current Vascular Pharmacology, 15, no. 2 (2017):115-122, https://doi.org/10.2174/1570161115666161104095522 . .