Microglial SLC25A28 Knockout Mitigates Spinal Cord Injury in Mice by Inhibiting Heme Synthesis and Subsequent NOX2 Activation.

ABSTRACT:

Background

Microglial overactivation-driven neuroinflammation exacerbates secondary damage after spinal cord injury (SCI), but the role of mitochondrial iron metabolism in this process is not well understood. This study investigates the function of the mitochondrial iron transporter solute carrier family 25 member 28 (SLC25A28) in post-SCI neuroinflammation.

Methods

Microglia-specific SLC25A28 knockout (A28-MGKO) mice were generated by crossing SLC25A28^flox/flox mice with Cx3cr1-CreERT2 mice and subjected to clip-compression spinal cord injury (SCI) at the T9 level. Motor recovery was evaluated using the Basso Mouse Scale (BMS), while histological and biochemical assessments including hematoxylin-eosin and Nissl staining, Iba1 immunohistochemistry, Evans blue perm

SUBMITTER: Chen H 

PROVIDER: S-EPMC12580241 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature