KLF13 restrains Dll4‐muscular Notch2 axis to improve the muscle atrophy
Autor: | Shu Yang, Lijiao Xiong, Guangyan Yang, Jiaqing Xiang, Lixing Li, Lin Kang, Zhen Liang |
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Jazyk: | angličtina |
Rok vydání: | 2024 |
Předmět: | |
Zdroj: | Journal of Cachexia, Sarcopenia and Muscle, Vol 15, Iss 5, Pp 1869-1882 (2024) |
Druh dokumentu: | article |
ISSN: | 2190-6009 2190-5991 |
DOI: | 10.1002/jcsm.13538 |
Popis: | 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 knockdown and RNA sequencing. Results In a dexamethasone‐induced muscle atrophy mouse model, the KLF13 knockout group had decreased muscle strength (N) (1.77 ± 0.10 vs. 1.48 ± 0.16, P |
Databáze: | Directory of Open Access Journals |
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