Acute central nervous system (CNS) injuries include stroke, traumatic brain injury, and spinal cord injury. Early brain injury is a main cause of disability and death for patients of stroke or traumatic brain injury. The mechanisms of early brain injury after stroke and trauma are complex, and remain poorly understood. Neuronal cell death in the acute phase of CNS injuries is a central pathological process, which determines the long-term neurological deficits and prognosis.
Apoptosis is the best-described form of programmed cell death. The mechanism of apoptosis is highly complex and sophisticated, including two main pathways: death receptor pathway and mitochondrial pathway. The two pathways are co-related and the molecules in pathways can influence the other’s pathological processes. Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. Under ordinary circumstance, autophagy serves as a stress adaptor that prevents cell death; whereas in other settings, it might constitute an alternative cell-death pathway. Autophagy activation after CNS injury could suppress apoptosis in a mutually exclusive manner. However, autophagy and apoptosis may be triggered by common upstream signals, resulting in programmed cell death without inflammatory reaction. Furthermore, the functional relationship between apoptosis and autophagy is complex, which depends on their different sensitivity thresholds. So, the balance between the apoptotic and autophagic response is critical to the fate of neuronal cell after CNS injuries.
This Research Topic attempts to further explain the two major pathophysiological processes of brain injury (apoptosis and autophagy), and explore the promising target for further therapeutic intervention. The purpose of this Research Topic is to present high-quality reviews and original research articles on apoptosis and autophagy in acute CNS injuries, as well as to confront the prospects and challenges.
Acute central nervous system (CNS) injuries include stroke, traumatic brain injury, and spinal cord injury. Early brain injury is a main cause of disability and death for patients of stroke or traumatic brain injury. The mechanisms of early brain injury after stroke and trauma are complex, and remain poorly understood. Neuronal cell death in the acute phase of CNS injuries is a central pathological process, which determines the long-term neurological deficits and prognosis.
Apoptosis is the best-described form of programmed cell death. The mechanism of apoptosis is highly complex and sophisticated, including two main pathways: death receptor pathway and mitochondrial pathway. The two pathways are co-related and the molecules in pathways can influence the other’s pathological processes. Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome. Under ordinary circumstance, autophagy serves as a stress adaptor that prevents cell death; whereas in other settings, it might constitute an alternative cell-death pathway. Autophagy activation after CNS injury could suppress apoptosis in a mutually exclusive manner. However, autophagy and apoptosis may be triggered by common upstream signals, resulting in programmed cell death without inflammatory reaction. Furthermore, the functional relationship between apoptosis and autophagy is complex, which depends on their different sensitivity thresholds. So, the balance between the apoptotic and autophagic response is critical to the fate of neuronal cell after CNS injuries.
This Research Topic attempts to further explain the two major pathophysiological processes of brain injury (apoptosis and autophagy), and explore the promising target for further therapeutic intervention. The purpose of this Research Topic is to present high-quality reviews and original research articles on apoptosis and autophagy in acute CNS injuries, as well as to confront the prospects and challenges.
