ArticleInternational journal of molecular sciences2020
P38α-MAPK Signaling Inhibition Attenuates Soleus Atrophy during Early Stages of Muscle Unloading.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Multi-omics identifies promoter methylation and gene expression changes associated with human skeletal muscle atrophy.Experimental physiology · 2026Article
- Skeletal muscle adaptation to microgravity: how altered mechanical cues drive catabolic signaling.EMBO reports · 2026Review
- Mitochondrial Impairment in Unloaded Postural Muscle: Mechanisms Driving Loss of Muscle Function and Mass.Antioxidants (Basel, Switzerland) · 2026Review
- Muscle Structure and Function Recovery: Adalimumab-Calcium Channel Synergy in Post-Ischemic Stroke Sarcopenia.Journal of cachexia, sarcopenia and muscle · 2025Article
- p38α MAPK Regulation of Energy Metabolism in Skeletal Muscle Offers a Therapeutic Path for Type 2 Diabetes.Cells · 2025Review
- Targeting MuRF1 to Combat Skeletal Muscle Wasting in Cardiac Cachexia: Mechanisms and Therapeutic Prospects.Medical science monitor : international medical journal of experimental and clinical research · 2024Review
- Palmitate-Induced Inflammation and Myotube Atrophy in C2C12 Cells Are Prevented by the Whey Bioactive Peptide, Glycomacropeptide.The Journal of nutrition · 2023Article
- The Effect of SERCA Activation on Functional Characteristics and Signaling of Rat Soleus Muscle upon 7 Days of Unloading.Biomolecules · 2023Article
- Effects of Various Muscle Disuse States and Countermeasures on Muscle Molecular Signaling.International journal of molecular sciences · 2021Review
- Plantar Mechanical Stimulation Maintains Slow Myosin Expression in Disused Rat Soleus Muscle via NO-Dependent Signaling.International journal of molecular sciences · 2021Article
- Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.Molecules (Basel, Switzerland) · 2021Review
- Molecular mechanisms of cancer cachexia‑induced muscle atrophy (Review).Molecular medicine reports · 2020Review
- MuRF1/TRIM63, Master Regulator of Muscle Mass.International journal of molecular sciences · 2020Review
- How Postural Muscle Senses Disuse? Early Signs and Signals.International journal of molecular sciences · 2020Review
- Differences in the Role of HDACs 4 and 5 in the Modulation of Processes Regulating MAFbx and MuRF1 Expression during Muscle Unloading.International journal of molecular sciences · 2020Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
To test the hypothesis that p38α-MAPK plays a critical role in the regulation of E3 ligase expression and skeletal muscle atrophy during unloading, we used VX-745, a selective p38α inhibitor. Three groups of rats were used: non-treated control (C), 3 days of unloading/hindlimb suspension (HS), and 3 days HS with VX-745 inhibitor (HSVX; 10 mg/kg/day). Total weight of soleus muscle in HS group was reduced compared to C (72.3 ± 2.5 vs 83.0 ± 3 mg, respectively), whereas muscle weight in the HSVX group was maintained (84.2 ± 5 mg). The expression of muscle RING-finger protein-1 (MuRF1) mRNA was significantly increased in the HS group (165%), but not in the HSVX group (127%), when compared with the C group. The expression of muscle-specific E3 ubiquitin ligases muscle atrophy F-box (MAFbx) mRNA was increased in both HS and HSVX groups (294% and 271%, respectively) when compared with C group. The expression of ubiquitin mRNA was significantly higher in the HS (423%) than in the C and HSVX (200%) groups. VX-745 treatment blocked unloading-induced upregulation of calpain-1 mRNA expression (HS: 120%; HSVX: 107%). These results indicate that p38α-MAPK signaling regulates MuRF1 but not MAFbx E3 ligase expression and inhibits skeletal muscle atrophy during early stages of unloading.
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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.