Ferroptosis is a recently defined iron-dependent non-apoptotic form of cell death. Diverse stressors can destabilize metabolic processes in the cell, leading to excessive intracellular accumulation of reactive oxygen species that culminate in the collapse and rupture of the membrane structure of cellular organelles, such as mitochondria, endoplasmic reticulum, and lysosome. Ferroptosis is a form of cell death characterized by the accumulation of intracellular iron and lipid ROS. The primary morphologic manifestations of ferroptosis include cell volume shrinkage and increased mitochondrial membrane density. These are different from apoptotic types of cell death such as necroptosis (early destruction of membrane integrity, cell and organelle swelling, cytoplasmic granulation and chromatin fragmentation, and cellular lysis), and pyroptosis (necrosis-like cell-membrane pore formation and rupture, cellular swelling, pro-inflammatory intracellular content release, as well as apoptosis-like nuclear condensation and DNA fragmentation).
Emerging evidence shows that ferroptosis has significant implications in neurological diseases such as stroke, traumatic brain injury (TBI), Alzheimer's disease and Parkinson's disease. Additionally, ferroptosis inhibition has been shown to protect neurons and ameliorate cognitive impairment in various disease animal models. To date, several ferroptosis inhibitors have been found. As Ferroptosis is characterized by the accumulation of intracellular iron and lipid ROS, these inhibitors are primarily categorized as either antioxidants or iron chelators. For example in hemorrhagic stroke, it was found that the neuronal death and iron deposition, induced by hemoglobin in organotypic hippocampal slice cultures and primary cortical neurons, can be attenuated by administration of ferrostatin-1, or other ferroptosis inhibitors.
In this Research Topic researchers are welcome to submit original research and review articles. We are interested in all topics associated with ferroptosis and neurological diseases, from underlying mechanisms to clinical transformation including potential targeting and treatment and others. We also welcome original articles analyzing similarities and differences among ferroptosis and other kinds of cell death, such as apoptosis and pyroptosis, in neurological diseases and hope to find key insights for future drug-development.
Ferroptosis is a recently defined iron-dependent non-apoptotic form of cell death. Diverse stressors can destabilize metabolic processes in the cell, leading to excessive intracellular accumulation of reactive oxygen species that culminate in the collapse and rupture of the membrane structure of cellular organelles, such as mitochondria, endoplasmic reticulum, and lysosome. Ferroptosis is a form of cell death characterized by the accumulation of intracellular iron and lipid ROS. The primary morphologic manifestations of ferroptosis include cell volume shrinkage and increased mitochondrial membrane density. These are different from apoptotic types of cell death such as necroptosis (early destruction of membrane integrity, cell and organelle swelling, cytoplasmic granulation and chromatin fragmentation, and cellular lysis), and pyroptosis (necrosis-like cell-membrane pore formation and rupture, cellular swelling, pro-inflammatory intracellular content release, as well as apoptosis-like nuclear condensation and DNA fragmentation).
Emerging evidence shows that ferroptosis has significant implications in neurological diseases such as stroke, traumatic brain injury (TBI), Alzheimer's disease and Parkinson's disease. Additionally, ferroptosis inhibition has been shown to protect neurons and ameliorate cognitive impairment in various disease animal models. To date, several ferroptosis inhibitors have been found. As Ferroptosis is characterized by the accumulation of intracellular iron and lipid ROS, these inhibitors are primarily categorized as either antioxidants or iron chelators. For example in hemorrhagic stroke, it was found that the neuronal death and iron deposition, induced by hemoglobin in organotypic hippocampal slice cultures and primary cortical neurons, can be attenuated by administration of ferrostatin-1, or other ferroptosis inhibitors.
In this Research Topic researchers are welcome to submit original research and review articles. We are interested in all topics associated with ferroptosis and neurological diseases, from underlying mechanisms to clinical transformation including potential targeting and treatment and others. We also welcome original articles analyzing similarities and differences among ferroptosis and other kinds of cell death, such as apoptosis and pyroptosis, in neurological diseases and hope to find key insights for future drug-development.
