The induction of ferroptosis in posthemorrhagic hydrocephalus

Posthemorrhagic hydrocephalus (PHH) is a common neurological disease characterized by the disordered secretion of cerebrospinal fluid from the choroid plexus, ventricular dilation, and increased intracranial pressure after hemorrhage. Although these pathological processes are well established, the effective biomarkers for the diagnosis of PHH are still limited, largely because the underlying mechanisms—including cell death in the choroid plexus—are not well defined. Ferroptosis, a newly recognized type of programmed cell death, has been found to play a key role in a variety of pathologic conditions and diseases, including Parkinson’s and Alzheimer’s diseases. However, whether ferroptosis is induced in PHH is still unknown. In the current study, a rat model of PHH was established to investigate the induction of ferroptosis in PHH. Along with defects in memory and cognition, we observed that rats with experimentally induced PHH also demonstrated lipid peroxidation (a key marker of ferroptosis), as well as a significant increase and a significant decrease in two ferroptosis-specific genes, ACSL4 and SLC7A11, respectively. Thus, ferroptosis may serve as an auxiliary indicator for the diagnosis of PHH.