FGF21 maintains redox homeostasis and promotes neuronal survival after traumatic brain injury by targeting SLC25A39-mediated mitochondrial GSH transport.

ABSTRACT:

Background

Traumatic brain injury (TBI) represents a critical form of acute brain injury, characterized by considerable mortality and morbidity. Recently, fibroblast growth factor 21 (FGF21), a multifaceted hormone predominantly synthesized in liver, has emerged as a promising neuroprotective agent. In the study, we aim to investigate whether FGF21 exerts protective effects against TBI and to further elucidate its underlying molecular mechanisms.

Methods

To elucidate the role of FGF21 in regulating SLC25A39-dependent mitochondrial GSH transport and providing protection against TBI-induced neurological deficits, a series of cellular and molecular techniques, including western blot analysis, real-time polymerase chain reaction, immunohistochemistry, transmission electron micro

SUBMITTER: Wang L 

PROVIDER: S-EPMC12492758 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature