ArticleJournal of applied physiology (Bethesda, Md. : 1985)2010
Skeletal muscle dysfunction in muscle-specific LKB1 knockout mice.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 44 citations in OpenAlex.
- The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025Review
- Chronic treatment of old mice with AICAR reverses age-related changes in exercise performance and skeletal muscle gene expression.FASEB bioAdvances · 2025Article
- Molecular pathways involved in the control of contractile and metabolic properties of skeletal muscle fibers as potential therapeutic targets for Duchenne muscular dystrophy.Frontiers in physiology · 2024Review
- Sarcopenic obesity: emerging mechanisms and therapeutic potential.Metabolism: clinical and experimental · 2023Review
- The Role of Autophagy in Skeletal Muscle Diseases.Frontiers in physiology · 2021Review
- Lack of skeletal muscle liver kinase B1 alters gene expression, mitochondrial content, inflammation and oxidative stress without affecting high-fat diet-induced obesity or insulin resistance.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- AMP-Activated Protein Kinase (AMPK) at the Crossroads Between COInternational journal of molecular sciences · 2020Review
- Insight on Transcriptional Regulation of the Energy Sensing AMPK and Biosynthetic mTOR Pathway Genes.Frontiers in cell and developmental biology · 2020Review
- Article
- The Role of AMPK in the Regulation of Skeletal Muscle Size, Hypertrophy, and Regeneration.International journal of molecular sciences · 2018Review
- Adipocyte-specific DKO of Lkb1 and mTOR protects mice against HFD-induced obesity, but results in insulin resistance.Journal of lipid research · 2018Article
- CXCL10 increases in human skeletal muscle following damage but is not necessary for muscle regeneration.Physiological reports · 2018Article
- AMPK in skeletal muscle function and metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Review
- Preclinical characterization of the JAK/STAT inhibitor SGI-1252 on skeletal muscle function, morphology, and satellite cell content.PloS one · 2018Article
- Deletion of Lkb1 in adult mice results in body weight reduction and lethality.Scientific reports · 2016Article
- Liver kinase B1 inhibits the expression of inflammation-related genes postcontraction in skeletal muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Deletion of Lkb1 in Renal Tubular Epithelial Cells Leads to CKD by Altering Metabolism.Journal of the American Society of Nephrology : JASN · 2016Article
- LKB1 deletion causes early changes in atrial channel expression and electrophysiology prior to atrial fibrillation.Cardiovascular research · 2015Article
- Lkb1 is indispensable for skeletal muscle development, regeneration, and satellite cell homeostasis.Stem cells (Dayton, Ohio) · 2014Article
- Regulation of (pro)renin receptor expression in mIMCD via the GSK-3β-NFAT5-SIRT-1 signaling pathway.American journal of physiology. Renal physiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Liver kinase B1 (LKB1) is a tumor-suppressing protein that is involved in the regulation of muscle metabolism and growth by phosphorylating and activating AMP-activated protein kinase (AMPK) family members. Here we report the development of a myopathic phenotype in skeletal and cardiac muscle-specific LKB1 knockout (mLKB1-KO) mice. The myopathic phenotype becomes overtly apparent at 30-50 wk of age and is characterized by decreased body weight and a proportional reduction in fast-twitch skeletal muscle weight. The ability to ambulate is compromised with an often complete loss of hindlimb function. Skeletal muscle atrophy is associated with a 50-75% reduction in mammalian target of rapamycin pathway phosphorylation, as well as lower peroxisome proliferator-activated receptor-alpha coactivator-1 content and cAMP response element binding protein phosphorylation (43 and 40% lower in mLKB1-KO mice, respectively). Maximum in situ specific force production is not affected, but fatigue is exaggerated, and relaxation kinetics are slowed in the myopathic mice. The increased fatigue is associated with a 30-78% decrease in mitochondrial protein content, a shift away from type IIA/D toward type IIB muscle fibers, and a tendency (P=0.07) for decreased capillarity in mLKB1-KO muscles. Hearts from myopathic mLKB1-KO mice exhibit grossly dilated atria, suggesting cardiac insufficiency and heart failure, which likely contributes to the phenotype. These findings indicate that LKB1 plays a critical role in the maintenance of both skeletal and cardiac function.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.