Inhibition of NOX4 attenuates muscle damage and mitochondrial dysfunction in inflammatory myopathy.

ABSTRACT:

Background

Idiopathic inflammatory myopathy (IIM) is a chronic autoimmune disorder characterized by muscle inflammation and weakness. If a muscle is already damaged, muscle strength often fails to restore with current treatments. Although, NADPH oxidase 4 (NOX4) is the main source of reactive oxygen species (ROS) and has been suggested to contribute to the pathogenesis of various disease by inducing ROS production and mitochondrial dysfunction, its role in IIM has not been fully explained.

Methods

Primary myoblasts from IIM patients and non-myopathic controls, as well as human skeletal muscle cells (SkMCs), were cultured under inflammatory conditions induced by interleukin (IL)-15, IL-6, and interferon-gamma (IFN-γ). NOX4 inhibitors, GKT137831 and GLX351322, were administere

SUBMITTER: Kang HR 

PROVIDER: S-EPMC12860102 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature