Ferroptosis and mitochondrial dysfunction in acute central nervous system injury

Abstract

Acute central nervous system injuries (ACNSI), encompassing traumatic brain injury (TBI), non-traumatic brain injury like stroke and encephalomeningitis, as well as spinal cord injuries, are linked to significant rates of disability and mortality globally. Nevertheless, effective and feasible treatment plans are still to be formulated. There are primary and secondary injuries occurred after ACNSI. Most ACNSIs exhibit comparable secondary injuries, which offer numerous potential therapeutic targets for enhancing clinical outcomes. Ferroptosis, a newly discovered form of cell death, is characterized as a lipid peroxidation process that is dependent on iron and oxidative conditions, which is also indispensable to mitochondria. Ferroptosis play a vital role in many neuropathological pathways, and ACNSIs may induce mitochondrial dysfunction, thereby indicating the essentiality of the mitochondrial connection to ferroptosis in ACNSIs. Nevertheless, there remains a lack of clarity regarding the involvement of mitochondria in the occurrence of ferroptosis as a secondary injuries of ACNSIs. In recent studies, anti-ferroptosis agents such as the ferroptosis inhibitor Ferrostain-1 and iron chelation therapy have shown potential in ameliorating the deleterious effects of ferroptosis in cases of traumatic ACNSI. The importance of this evidence is extremely significant in relation to the research and control of ACNSIs. Therefore, our review aims to provide researchers focusing on enhancing the therapeutic outcomes of ACNSIs with valuable insights by summarizing the physiopathological mechanisms of ACNSIs and exploring the correlation between ferroptosis, mitochondrial dysfunction, and ACNSIs.

New insights into the spleen injury by mitochondrial dysfunction of chicken under polystyrene microplastics stress

“…Under external stimuli, the cell death signal is transmitted to mitochondria, B-cell lymphoma-2 ( Bcl-2 ) family mediates the opening of membrane permeability transition pore and the efflux of cytochrome c ( cytc ), which initiates the mitochondrial apoptosis pathway ( Martinou and Youle 2011 ; Wang et al, 2021 ). Ferroptosis is an iron dependence of programmed cell death, in which mitochondria have been found to play a crucial part ( Dong et al, 2023 ; Li et al, 2023c ). Mitochondria participate in the regulation of the body's redox equilibrium.…”