Bench-to-bedside review: Apoptosis/programmed cell death triggered by traumatic brain injury
نویسندگان
چکیده
Apoptosis, or programmed cell death, is a physiological form of cell death that is important for normal embryologic development and cell turnover in adult organisms. Cumulative evidence suggests that apoptosis can also be triggered in tissues without a high rate of cell turnover, including those within the central nervous system (CNS). In fact, a crucial role for apoptosis in delayed neuronal loss after both acute and chronic CNS injury is emerging. In the current review we summarize the growing evidence that apoptosis occurs after traumatic brain injury (TBI), from experimental models to humans. This includes the identification of apoptosis after TBI, initiators of apoptosis, key modulators of apoptosis such as the Bcl-2 family, key executioners of apoptosis such as the caspase family, final pathways of apoptosis, and potential therapeutic interventions for blocking neuronal apoptosis after TBI.
منابع مشابه
Bench-to-bedside review: Mitochondrial injury, oxidative stress and apoptosis – there is nothing more practical than a good theory
Apoptosis contributes to cell death in common intensive care unit disorders such as traumatic brain injury and sepsis. Recent evidence suggests that this form of cell death is both clinically relevant and a potential therapeutic target in critical illness. Mitochondrial reactive oxygen species (ROS) have become a target for drug discovery in recent years since their production is characteristic...
متن کاملMelatonin treatment reduces astrogliosis and apoptosis in rats with traumatic brain injury
Objective(s):Melatonin is known as an anti-inflammatory agent, and it has been proven to exert neuroprotection through inhibition of cell death (apoptosis) in several models of brain injury.Secondary injury following the primary traumatic brain injury (TBI) results in glial cells activation, especially astrocytes. In fact, astrocyte activation causes the production of pro-inflammatory cytokines...
متن کاملImpact of Duration and Severity of Persistent Pain on Programmed Cell Death
Programmed cell death is a highly regulated form of cell death, mostly distinguished by the activation of a family of cystein-aspartate proteases (caspases) that cleave various proteins resulting in morphological and biochemical changes characteristic of this form of cell death. Several recent studies have addressed the role of programmed cell death in inflammatory and chronic pain states. Casp...
متن کاملImpact of Duration and Severity of Persistent Pain on Programmed Cell Death
Programmed cell death is a highly regulated form of cell death, mostly distinguished by the activation of a family of cystein-aspartate proteases (caspases) that cleave various proteins resulting in morphological and biochemical changes characteristic of this form of cell death. Several recent studies have addressed the role of programmed cell death in inflammatory and chronic pain states. Casp...
متن کاملIncreases in Bcl-2 and cleavage of caspase-1 and caspase-3 in human brain after head injury.
The bcl-2 and caspase families are important regulators of programmed cell death in experimental models of ischemic, excitotoxic, and traumatic brain injury. The Bcl-2 family members Bcl-2 and Bcl-xL suppress programmed cell death, whereas Bax promotes programmed cell death. Activated caspase-1 (interleukin-1beta converting enzyme) and caspase-3 (Yama/Apopain/Cpp32) cleave proteins that are imp...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Critical Care
دوره 9 شماره
صفحات -
تاریخ انتشار 2005