Special Issue "Ferroptosis and Its Potential Role in the Physiopathology of Brain Injury"
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 7007
Interests: brain injury; traumatic brain injury; cognitive function; ferroptosis; cell death; mitochondrion; oxidative stress; neuroinflammation; forensic pathology
As a novel mode of regulated cell death, ferroptosis has distinctive morphological and biochemical features, including morphological changes in mitochondria, the accumulation of iron, and lipid reactive oxygen species (ROS). Studies at present have shown that disturbances to iron homeostasis, lipid ROS accumulation, and other manifestations related to ferroptosis can be detected in brain injury, suggesting that ferroptosis may play an important role in the physiopathology of brain injury, such as traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), ischemia/reperfusion injury, and hypoxic–ischemic injury.
We invite you to submit your latest original research findings or a review article to this Special Issue, which will bring together current research concerning the molecular mechanisms and potential roles of ferroptosis in the physiopathology of brain injury. This research can include both in vitro and in vivo studies relating to, but not limited to, any of the following topics: activation/inhibition mechanism of molecular mediators of ferroptosis after brain injury; modulation of signaling pathways of ferroptosis in brain injury; the relationship between ferroptosis and other mechanisms such as neuroinflammation and autophagy after brain injury; modulation of ferroptosis molecular mediators of brain injury; and the potential roles of ferroptosis in cognitive dysfunction caused by brain injury.
We look forward to your contribution.
Dr. Chengliang Luo
Manuscript Submission Information
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- brain injury
- cell death
- lipid peroxidation
- iron homeostasis