ArticleDisease models & mechanisms2023
LKB1 signaling is altered in skeletal muscle of a Duchenne muscular dystrophy mouse model.
Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- LKB1 Dysregulation in Duchenne Muscular Dystrophy Models: Disease Specificity and Epigenetic Control by HDAC Inhibitors.Annals of the New York Academy of Sciences · 2026Article
- Best reference genes for unbiased normalized transcript expression in normal and dystrophic human cell models of myogenesis.PloS one · 2026Article
- Volitional exercise elicits physiological and molecular improvements in the severe D2.mdx mouse model of Duchenne muscular dystrophy.The Journal of physiology · 2026Article
- From Symptomatic Therapies to Disease-Modifying Approaches for Neuronal Sodium Channel Disorders.International journal of molecular sciences · 2025Review
- Patient-Oriented In Vitro Studies in Duchenne Muscular Dystrophy: Validation of a 3D Skeletal Muscle Organoid Platform.Biomedicines · 2025Article
- The SIRT1 activator SRT2104 exerts exercise mimetic effects and promotes Duchenne muscular dystrophy recovery.Cell death & disease · 2025Article
- Therapeutic Approaches to Tuberous Sclerosis Complex: From Available Therapies to Promising Drug Targets.Biomolecules · 2024Review
- Article
- Branched-chain amino acids and L-alanine supplementation ameliorate calcium dyshomeostasis in sarcopenia: New insights for nutritional interventions.Frontiers in pharmacology · 2024Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The potential role of liver kinase B1 (LKB1) in the altered activation of the master metabolic and epigenetic regulator adenosine monophosphate-activated protein kinase (AMPK) in Duchenne muscular dystrophy has not been investigated so far. Hence, we analyzed both gene and protein levels of LKB1 and its related targets in gastrocnemius muscles of adult C57BL/10 mdx mice and D2 mdx mice, a model with a more severe dystrophic phenotype, as well as the sensitivity of the LKB1-AMPK pathway to AMPK activators, such as chronic exercise. Our data show, for the first time, a reduction in the levels of LKB1 and accessory proteins, MO25 and STRADα, in both mdx strains versus the respective wild type, which was further impaired by exercise, in parallel with a lack of further phosphorylation of AMPK. The AMPK-like kinase salt-inducible kinase (SIK) and class II histone deacetylases, along with expression of the HDAC target gene Mef2c, were also altered, supporting an impairment of LKB1-SIK-class II histone deacetylase signaling. Our results demonstrate that LKB1 may be involved in dystrophic progression, paving the way for future preclinical studies.
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