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Published on: October 27, 2020
Regulation of myogenic activation of p38 MAPK by TACE-mediated TNFα release
Yi-Ping Li1, Airu Niu1, Yefei Wen1
1Department of Integrative Biology and Pharmacology, University of Texas Health Science Center Houston, TX, USA.
Abstract:
The activation of p38 MAPK in myogenic precursor cells (MPCs) is a key signal for their exit of cell cycle and entry of the myogenic differentiation program. Therefore, identification of the signaling mechanism that activates p38 MAPK during this process is important for the understanding of the regulatory mechanism of muscle regeneration. This article reviews recent findings regarding the role of inflammatory cytokine tumor necrosis factor-α (TNFα) as a key activator of p38 MAPK during myogenesis in an autocrine/paracrine fashion, and the signaling mechanisms that converge upon TNFα converting enzyme (TACE) to release TNFα from differentiating MPCs in response to diverse regenerative stimuli.
Insights
Tumor necrosis factor-alpha (TNFα) activates p38 MAPK, a key signal for muscle regeneration. This review explores how TNFα is released to promote myogenesis and muscle repair.
Area of Science:
- Muscle regeneration
- Cell signaling
- Molecular biology
Background:
- p38 MAPK activation is crucial for myogenic precursor cells (MPCs) to exit the cell cycle and initiate differentiation.
- Understanding the signaling pathways that activate p38 MAPK is vital for elucidating muscle regeneration mechanisms.
Purpose of the Study:
- To review recent findings on the role of tumor necrosis factor-alpha (TNFα) in activating p38 MAPK during myogenesis.
- To explore the signaling mechanisms that lead to TNFα release from differentiating MPCs.
Main Methods:
- Literature review of recent research findings.
- Analysis of signaling pathways involving TNFα and TACE.
- Focus on autocrine/paracrine signaling in MPCs.
Main Results:
- TNFα acts as a key activator of p38 MAPK in MPCs during myogenesis.
- TNFα functions in both autocrine and paracrine manners.
- Diverse regenerative stimuli converge on TNFα converting enzyme (TACE) to release TNFα.
Conclusions:
- TNFα signaling is a central mechanism in p38 MAPK activation during muscle regeneration.
- TACE-mediated release of TNFα is a critical step in response to regenerative cues.
- Further understanding of this pathway can inform strategies for enhancing muscle repair.
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