ArticleSkeletal muscle2017
Loss of MKP-5 promotes myofiber survival by activating STAT3/Bcl-2 signaling during regenerative myogenesis.
Article in Skeletal muscle, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Mitochondrial stress response and myogenic differentiation.Frontiers in cell and developmental biology · 2024Review
- Mitochondrial dysfunction: roles in skeletal muscle atrophy.Journal of translational medicine · 2023Review
- Defining the structure-activity relationship for a novel class of allosteric MKP5 inhibitors.European journal of medicinal chemistry · 2022Article
- Skeletal Muscle Regeneration in Cardiotoxin-Induced Muscle Injury Models.International journal of molecular sciences · 2022Review
- Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells.Oncology letters · 2020Article
- The Role of MKP-5 in Adipocyte-Macrophage Interactions during Obesity.Obesity facts · 2020Article
- Role of dual-specificity protein phosphatase DUSP10/MKP-5 in pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Muscle Injury Associated Elevated Oxidative Stress and Abnormal Myogenesis in Patients with Idiopathic Scoliosis.International journal of biological sciences · 2019Article
- Dual-specificity MAP kinase phosphatases in health and disease.Biochimica et biophysica acta. Molecular cell research · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe mitogen-activated protein kinases (MAPKs) have been shown to be involved in regulating myofiber survival. In skeletal muscle, p38 MAPK and JNK are negatively regulated by MAPK phosphatase-5 (MKP-5). During muscle regeneration, MKP-5 is downregulated, thereby promoting p38 MAPK/JNK signaling, and subsequent repair of damaged muscle. Mice lacking MKP-5 expression exhibit enhanced regenerative myogenesis. However, the effect of MKP-5 on myofiber survival during regeneration is unclear.
methodsTo investigate whether MKP-5 is involved in myofiber survival, skeletal muscle injury was induced by cardiotoxin injection, and the effects on apoptosis were assessed by TUNEL assay in wild type and MKP-5-deficient mice. The contribution of MKP-5 to apoptotic signaling and its link to this pathway through mitochondrial function were determined in regenerating skeletal muscle of MKP-5-deficient mice.
resultsWe found that loss of MKP-5 in skeletal muscle resulted in improved myofiber survival. In response to skeletal muscle injury, loss of MKP-5 decreased activation of the mitochondrial apoptotic pathway involving the signal transducer and activator of transcription 3 (STAT3) and increased expression of the anti-apoptotic transcription factor Bcl-2. Skeletal muscle of MKP-5-deficient mice also exhibited an improved anti-oxidant capacity as a result of increased expression of catalase further contributing to myofiber survival by attenuating oxidative damage.
conclusionsTaken together, these findings suggest that MKP-5 coordinates skeletal muscle regeneration by regulating mitochondria-mediated apoptosis. MKP-5 negatively regulates apoptotic signaling, and during regeneration, MKP-5 downregulation contributes to the restoration of myofiber survival. Finally, these results suggest that MKP-5 inhibition may serve as an important therapeutic target for the preservation of skeletal muscle survival in degenerative muscle diseases.
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