Understanding the contribution of iron in traumatic brain injury (TBI)

Abstract

Traumatic brain injury (TBI) is a socioeconomic burden and the underlying mechanisms that govern iron homeostasis after TBI is not fully elucidated. Evidently, iron accumulation observed after injury can contribute to the exacerbation of cellular consequences. Yet, the iron content observed might not all originate from haemorrhage, as non-heme iron is also evident. Interestingly, the alterations of iron-regulatory proteins such as amyloid precursor protein (APP), ceruloplasmin (CP), ferritin (Ft) and ferroportin (Fpn) may all be contributing factors to iron dyshomeostasis after TBI. Therefore, understanding the contribution of iron after TBI can deepen our understanding of iron-regulation and assist in the development of therapeutics to target iron-related insults after injury.