ArticleAmerican journal of physiology. Cell physiology2007
TNF-alpha regulates myogenesis and muscle regeneration by activating p38 MAPK.
Article in American journal of physiology. Cell physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.
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Who cites it
160 citing papers in PubMed, 290 citations in OpenAlex.
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- Cytokine Gene Variants Are Associated With Aerobic Fitness-Related, Hematological, and Metabolic Traits in Healthy Adults.Comprehensive Physiology · 2026Article
- Enhancers integrate microenvironmental signals in muscle stem cells during regeneration in health, disease, and aging.Skeletal muscle · 2026Review
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- Pro-inflammatory cytokine-driven molecular signaling in skeletal muscle during cancer cachexia.Biochemical Society transactions · 2026Review
- Dual Roles of Adipose Tissue in Skeletal Muscle Regeneration: Pro-Regenerative Versus Maladaptive.Journal of cachexia, sarcopenia and muscle · 2026Review
- Defective plasticity in dermatomyositis patients muscle stem cells is associated with sustained intrinsic inflammatory signaling and disruption of the histone H3.3 chromatin loading pathway.NAR molecular medicine · 2026Article
- ASB5 is a specific marker for muscle satellite cells but dispensable for skeletal muscle development and regeneration.Skeletal muscle · 2026Article
- Chronic macrophage activation derails muscle repair by disrupting mannose-receptor-linked plasticity revealed by endogenous irg1/acod1 tracking.Nature communications · 2026Article
- The Inflammation-Energy Metabolism Axis: A Central Driver of Sarcopenia-Osteoporosis: A Narrative Review.Calcified tissue international · 2026Review
- Ageing-Associated Dysregulation of Myogenic Differentiation in Inclusion Body Myositis.Journal of cachexia, sarcopenia and muscle · 2026Review
- A review: oxidative stress in skeletal muscle and the non-coding RNAs behind it.Molecular and cellular biochemistry · 2025Review
- Sarcopenia in Rheumatic Diseases: A Hidden Issue of Concern.Diseases (Basel, Switzerland) · 2025Review
100 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although p38 MAPK activation is essential for myogenesis, the upstream signaling mechanism that activates p38 during myogenesis remains undefined. We recently reported that p38 activation, myogenesis, and regeneration in cardiotoxin-injured soleus muscle are impaired in TNF-alpha receptor double-knockout (p55(-/-)p75(-/-)) mice. To fully evaluate the role of TNF-alpha in myogenic activation of p38, we tried to determine whether p38 activation in differentiating myoblasts requires autocrine TNF-alpha, and whether forced activation of p38 rescues impaired myogenesis and regeneration in the p55(-/-)p75(-/-) soleus. We observed an increase of TNF-alpha release from C2C12 or mouse primary myoblasts placed in low-serum differentiation medium. A TNF-alpha-neutralizing antibody added to differentiation medium blocked p38 activation and suppressed differentiation markers myocyte enhancer factor (MEF)-2C, myogenin, p21, and myosin heavy chain in C2C12 myoblasts. Conversely, recombinant TNF-alpha added to differentiation medium stimulated myogenesis at 0.05 ng/ml while inhibited it at 0.5 and 5 ng/ml. In addition, differentiation medium-induced p38 activation and myogenesis were compromised in primary myoblasts prepared from p55(-/-)p75(-/-) mice. Increased TNF-alpha release was also seen in cardiotoxin-injured soleus over the course of regeneration. Forced activation of p38 via the constitutive activator of p38, MKK6bE, rescued impaired myogenesis and regeneration in the cardiotoxin-injured p55(-/-)p75(-/-) soleus. These results indicate that TNF-alpha regulates myogenesis and muscle regeneration as a key activator of p38.
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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.