ArticleThe Journal of clinical investigation2009
MAPK phosphatase-1 facilitates the loss of oxidative myofibers associated with obesity in mice.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- MAP kinase phosphatases in metabolic diseases.Trends in endocrinology and metabolism: TEM · 2026Review
- Multi-Omics Insights into Postnatal Skeletal Muscle Development in Duroc Pigs.Animals : an open access journal from MDPI · 2025Article
- P38α MAPK Coordinates Mitochondrial Adaptation to Caloric Surplus in Skeletal Muscle.International journal of molecular sciences · 2024Article
- The influence of biological sex in human skeletal muscle transcriptome during ageing.Biogerontology · 2024Article
- Skeletal muscle TET3 promotes insulin resistance through destabilisation of PGC-1α.Diabetologia · 2024Article
- Construction of a co-expression network affecting intramuscular fat content and meat color redness based on transcriptome analysis.Frontiers in genetics · 2024Article
- Protein Kinases in Obesity, and the Kinase-Targeted Therapy.Advances in experimental medicine and biology · 2024Review
- MKP1 promotes nonalcoholic steatohepatitis by suppressing AMPK activity through LKB1 nuclear retention.Nature communications · 2023Article
- Identification of key immune-related genes and immune infiltration in diabetic nephropathy based on machine learning algorithms.IET systems biology · 2023Article
- Liver Injury and Metabolic Dysregulation in Largemouth Bass (Metabolites · 2023Article
- Supplementation withNutrients · 2022Article
- Screening of Genes Related to Growth, Development and Meat Quality of Sahan Crossbred F1 Sheep Based on RNA-Seq Technology.Frontiers in veterinary science · 2022Article
- p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?International journal of molecular sciences · 2020Review
- MKP-1 Modulates Mitochondrial Transcription Factors, Oxidative Phosphorylation, and Glycolysis.ImmunoHorizons · 2020Article
- Exploiting Common Aspects of Obesity and Alzheimer's Disease.Frontiers in human neuroscience · 2020Review
- Improving Obesity and Insulin Resistance by Targeting Skeletal Muscle MKP-1.Journal of cellular signaling · 2020Article
- Dual-specificity phosphatases regulate mitogen-activated protein kinase signaling in adipocytes in response to inflammatory stress.Cellular signalling · 2019Article
- Dual-specificity MAP kinase phosphatases in health and disease.Biochimica et biophysica acta. Molecular cell research · 2019Review
- Identification of single nucleotide polymorphisms ofJournal of animal science and biotechnology · 2019Article
- Skeletal Muscle-Specific Deletion of MKP-1 Reveals a p38 MAPK/JNK/Akt Signaling Node That Regulates Obesity-Induced Insulin Resistance.Diabetes · 2018Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Oxidative myofibers, also known as slow-twitch myofibers, help maintain the metabolic health of mammals, and it has been proposed that decreased numbers correlate with increased risk of obesity. The transcriptional coactivator PPARgamma coactivator 1alpha (PGC-1alpha) plays a central role in maintaining levels of oxidative myofibers in skeletal muscle. Indeed, loss of PGC-1alpha expression has been linked to a reduction in the proportion of oxidative myofibers in the skeletal muscle of obese mice. MAPK phosphatase-1 (MKP-1) is encoded by mkp-1, a stress-responsive immediate-early gene that dephosphorylates MAPKs in the nucleus. Previously we showed that mice deficient in MKP-1 have enhanced energy expenditure and are resistant to diet-induced obesity. Here we show in mice that excess dietary fat induced MKP-1 overexpression in skeletal muscle, and that this resulted in reduced p38 MAPK-mediated phosphorylation of PGC-1alpha on sites that promoted its stability. Consistent with this, MKP-1-deficient mice expressed higher levels of PGC-1alpha in skeletal muscle than did wild-type mice and were refractory to the loss of oxidative myofibers when fed a high-fat diet. Collectively, these data demonstrate an essential role for MKP-1 as a regulator of the myofiber composition of skeletal muscle and suggest a potential role for MKP-1 in metabolic syndrome.
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