ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2014
Muscle-specific AMPK β1β2-null mice display a myopathy due to loss of capillary density in nonpostural muscles.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- AMPK as a mediator of tissue preservation: time for a shift in dogma?Nature reviews. Endocrinology · 2024Review
- Mechanisms and effects of metformin on skeletal muscle disorders.Frontiers in neurology · 2023Review
- Wheel running improves fasting-induced AMPK signaling in skeletal muscle from tumor-bearing mice.Physiological reports · 2021Article
- MetforminFrontiers in physiology · 2021Article
- Sarcopenia and Muscle Aging: A Brief Overview.Endocrinology and metabolism (Seoul, Korea) · 2020Review
- The role of neutrophil extracellular traps and TLR signaling in skeletal muscle ischemia reperfusion injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- AMPK Complex Activation Promotes Sarcolemmal Repair in Dysferlinopathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2020Article
- AMP-activated protein kinase: the current landscape for drug development.Nature reviews. Drug discovery · 2019Review
- Overexpression of miR-29 Leads to Myopathy that Resemble Pathology of Ullrich Congenital Muscular Dystrophy.Cells · 2019Article
- The Role of AMPK in the Regulation of Skeletal Muscle Size, Hypertrophy, and Regeneration.International journal of molecular sciences · 2018Review
- AMPK in skeletal muscle function and metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Review
- Exercise-stimulated glucose uptake - regulation and implications for glycaemic control.Nature reviews. Endocrinology · 2017Review
- Article
- Functional characterization of AMP-activated protein kinase signaling in tumorigenesis.Biochimica et biophysica acta · 2016Review
- Liver kinase B1 inhibits the expression of inflammation-related genes postcontraction in skeletal muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Dystrophin-glycoprotein complex regulates muscle nitric oxide production through mechanoregulation of AMPK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- AMPK deficiency in cardiac muscle results in dilated cardiomyopathy in the absence of changes in energy metabolism.Cardiovascular research · 2015Article
- mTOR signaling in tumorigenesis.Biochimica et biophysica acta · 2014Review
- Contraction-stimulated glucose transport in muscle is controlled by AMPK and mechanical stress but not sarcoplasmatic reticulum Ca(2+) release.Molecular metabolism · 2014Article
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
AMP-activated protein kinase (AMPK) is a master regulator of metabolism. While muscle-specific AMPK β1β2 double-knockout (β1β2M-KO) mice display alterations in metabolic and mitochondrial capacity, their severe exercise intolerance suggested a secondary contributor to the observed phenotype. We find that tibialis anterior (TA), but not soleus, muscles of sedentary β1β2M-KO mice display a significant myopathy (decreased myofiber areas, increased split and necrotic myofibers, and increased centrally nucleated myofibers. A mitochondrial- and fiber-type-specific etiology to the myopathy was ruled out. However, β1β2M-KO TA muscles displayed significant (P<0.05) increases in platelet aggregation and apoptosis within myofibers and surrounding interstitium (P<0.05). These changes correlated with a 45% decrease in capillary density (P<0.05). We hypothesized that the β1β2M-KO myopathy in resting muscle resulted from impaired AMPK-nNOSμ signaling, causing increased platelet aggregation, impaired vasodilation, and, ultimately, ischemic injury. Consistent with this hypothesis, AMPK-specific phosphorylation (Ser1446) of nNOSμ was decreased in β1β2M-KO compared to wild-type (WT) mice. The AMPK-nNOSμ relationship was further demonstrated by administration of 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR) to β1β2-MKO muscles and C2C12 myotubes. AICAR significantly increased nNOSμ phosphorylation and nitric oxide production (P<0.05) within minutes of administration in WT muscles and C2C12 myotubes but not in β1β2M-KO muscles. These findings highlight the importance of the AMPK-nNOSμ pathway in resting skeletal muscle.
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