APE1/Ref-1 inhibition via APX3330 lowers monocyte/macrophage infiltration without ameliorating the structure and function of dystrophic mdx hindlimb muscles.

ABSTRACT: Chronic inflammation and oxidative stress exacerbate muscle wasting and weakness in Duchenne muscular dystrophy (DMD). Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) regulates transcription factors involved in inflammatory and oxidative stress pathways. APE1/Ref-1 is an emerging therapeutic target in inflammatory conditions. This study aimed to investigate the effects of APX3330, a small molecule inhibitor of APE1's Ref-1 on mdx mouse pathology, a model of DMD. Six-week-old mdx mice and wild type (WT) C57Bl/10 mice were treated with APX3330 (25 mg·kg^-1) or vehicle for 6 weeks. Ex vivo contractile function, histological and biochemical analysis were performed in extensor digitorum longus (EDL) and soleus muscles. APE1/Ref-1 protein was greater in mdx hindlimb mu

SUBMITTER: Lalunio H 

PROVIDER: S-EPMC12314421 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature