Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.

Spontaneous subarachnoid hemorrhage (SAH), mainly caused by ruptured intracranial aneurysms, is a serious acute cerebrovascular disease. Early brain injury (EBI) is all brain injury occurring within 72 h after SAH, mainly including increased intracranial pressure, decreased cerebral blood flow, disruption of the blood-brain barrier, brain edema, oxidative stress, and neuroinflammation. It activates cell death pathways, leading to neuronal and glial cell death, and is significantly associated with poor prognosis. Ferroptosis is characterized by iron-dependent accumulation of lipid peroxides and is involved in the process of neuron and glial cell death in early brain injury. This paper reviews the research progress of ferroptosis in early brain injury after subarachnoid hemorrhage and provides new ideas for future research.

A Novel Six Autophagy-Related Genes Signature Associated With Outcomes and Immune Microenvironment in Lower-Grade Glioma.

Since autophagy and the immune microenvironment are deeply involved in the tumor development and progression of Lower-grade gliomas (LGG), our study aimed to construct an autophagy-related risk model for prognosis prediction and investigate the relationship between the immune microenvironment and risk signature in LGG. Therefore, we identified six autophagy-related genes (BAG1, PTK6, EEF2, PEA15, ITGA6, and MAP1LC3C) to build in the training cohort (n = 305 patients) and verify the prognostic model in the validation cohort (n = 128) and the whole cohort (n = 433), based on the data from The Cancer Genome Atlas (TCGA). The six-gene risk signature could divide LGG patients into high- and low-risk groups with distinct overall survival in multiple cohorts (all p < 0.001). The prognostic effect was assessed by area under the time-dependent ROC (t-ROC) analysis in the training, validation, and whole cohorts, in which the AUC value at the survival time of 5 years was 0.837, 0.755, and 0.803, respectively. Cox regression analysis demonstrated that the risk model was an independent risk predictor of OS (HR > 1, p < 0.05). A nomogram including the traditional clinical parameters and risk signature was constructed, and t-ROC, C-index, and calibration curves confirmed its robust predictive capacity. KM analysis revealed a significant difference in the subgroup analyses' survival. Functional enrichment analysis revealed that these autophagy-related signatures were mainly involved in the phagosome and immune-related pathways. Besides, we also found significant differences in immune cell infiltration and immunotherapy targets between risk groups. In conclusion, we built a powerful predictive signature and explored immune components (including immune cells and emerging immunotherapy targets) in LGG.