Editorial: Ferroptosis in stroke, neurotrauma and neurodegeneration, volume II

Ferroptosis, a new form of cell death, is characterized by the accumulation of intracellular iron and lipid reactive oxygen species (ROS) [1]. The primary morphologic manifestations of ferroptosis include cell volume shrinkage and increased mitochondrial membrane density. This process of ferroptosis differs from other apoptotic types of cell death such as necroptosis and pyroptosis [2]. Growing evidence indicates that ferroptosis plays key roles in neurological diseases such as stroke, traumatic brain injury (TBI), and neurodegenerative diseases (Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), vascular dementia (VD), Huntington's disease (HD)) [2,3].Ferroptosis inhibition has been shown to protect neurons and ameliorate cognitive impairment in various disease animal models [4,5]. However, to date, the underlying mechanisms that how ferroptosis causes neurological injuries are still unclear. This collection finally published nine studies, which extensively explored the relationships between ferroptosis and neurological diseases (stroke, TBI, and neurodegenerative diseases), including underlying mechanisms of ferroptosis, potential targeting, and the relationship between ferroptosis and other kinds of cell death (necroptosis and pyroptosis).Zhu et al. adopted the method of bioinformatics analysis to explore the ferroptosis-related ceRNA regulation network in intracranial aneurysm. These studies extensively demonstrated the underlying mechanisms of ferroptosis in stroke and its potential therapeutic targets, which provides key information for future study of ferroptosis in stroke.Among the rest, three studies emphasized the important roles of ferroptosis in neurodegenerative diseases. Wang et al. applied bioinformatic analysis to explore ferroptosis-related biomarkers for AD.They also analyzed the data from GEO datasets and performed enrichment analyses of protein-protein interaction (PPI), the Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Twentyfour ferroptosis-related genes were identified as target genes. The remaining two studies provided another view of neuronal death in neurological diseases.