Type 3 deiodinase activation mediated by the Shh/Gli1 axis promotes sepsis-induced metabolic dysregulation in skeletal muscles.

ABSTRACT:

Background

Non-thyroidal illness syndrome is commonly observed in critically ill patients, characterized by the inactivation of systemic thyroid hormones (TH), which aggravates metabolic dysfunction. Recent evidence indicates that enhanced TH inactivation is mediated by the reactivation of type 3 deiodinase (Dio3) at the tissue level, culminating in a perturbed local metabolic equilibrium. This study assessed whether targeted inhibition of Dio3 can maintain tissue metabolic homeostasis under septic conditions and explored the mechanism behind Dio3 reactivation.

Methods

A retrospective clinical study was conducted to investigate the attributes of rT3. The expression of Dio3 was detected by immunoblotting, immunofluorescence, and immunohistochemical staining in tissues extract

SUBMITTER: Wang G 

PROVIDER: S-EPMC11773416 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature