KLF13 restrains Dll4-muscular Notch2 axis to improve the muscle atrophy.

ABSTRACT:

Background

Muscle atrophy can cause muscle dysfunction and weakness. Krüppel-like factor 13 (KLF13), a central regulator of cellular energy metabolism, is highly expressed in skeletal muscles and implicated in the pathogenesis of several diseases. This study investigated the role of KLF13 in muscle atrophy, which could be a novel therapeutic target.

Methods

The effects of gene knockdown and pharmacological targeting of KLF13 on skeletal muscle atrophy were investigated using cell-based and animal models. Clofoctol, an antibiotic and KLF13 agonist, was also investigated as a candidate for repurposing. The mechanisms related to skeletal muscle atrophy were assessed by measuring the expression levels and activation statuses of key regulatory pathways and validated using gene kn

SUBMITTER: Yang S 

PROVIDER: S-EPMC11446702 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature