Exercise, MAPK, and NF-κB signaling in skeletal muscle
Abstract
Mitogen-activated protein kinases (MAPKs) and NF-κB are two major regulators of gene transcription and metabolism in response to oxidative, energetic, and mechanical stress in skeletal muscle. Chronic activation of these signaling pathways has been implicated in the development and perpetuation of various pathologies, such as diabetes and cachexia. However, both MAPK and NF-κB are also stimulated by exercise, which promotes improvements in fuel homeostasis and can prevent skeletal muscle atrophy. This review will first discuss the major MAPK signaling modules in skeletal muscle, their differential activation by exercise, and speculated functions on acute substrate metabolism and exercise-induced gene expression. Focus will then shift to examination of the NF-κB pathway, including its mechanism of activation by cellular stress and its putative mediation of exercise-stimulated adaptations in antioxidant status, tissue regeneration, and metabolism. Although limited, there is additional evidence to suggest cross talk between MAPK and NF-κB signals with exercise. The objectives herein are twofold: 1) to determine how and why exercise activates MAPK and NF-κB; and 2) to resolve their paradoxical activation during diseased and healthy conditions.
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The MAPK cascade(s), particularly ERK1/2, play a dual role in myogenesis.
“The MAPK cascade(s), particularly the extracellular signal-regulated kinases (ERK) 1 and 2 (ERK1/2), play a duel role in myogenesis [125,126].”
From Potential Roles of n-3 PUFAs during Skeletal Muscle Growth and Regeneration (2018) · cites this paper as [126]
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- Authors
- Kramer, H. F., & Goodyear, L. J.
- Affiliations
- Brigham and Women's Hospital (US)
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2007-07
- Volume
- 103
- Issue
- 1
- Pages
- 388-395
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2157306000
- Cited by
- 375
- References
- 102
- Citations by year
- 2026: 15 · 2025: 15 · 2024: 24 · 2023: 23 · 2022: 28 · 2021: 19 · 2020: 17 · 2019: 11 · 2018: 13 · 2017: 19 · 2016: 21 · 2015: 18 · 2014: 19 · 2013: 23 · 2012: 25
- FWCI
- 2.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- physical activity, mitogen-activated protein kinase, NF-κB signaling, skeletal muscle, skeletal muscle atrophy, fuel homeostasis, substrate metabolism, exercise-induced gene expression, antioxidant status, muscle regeneration, diabetes mellitus, cachexia, cellular stress
- MeSH terms
- Adaptation, Physiological, Animals, Energy Metabolism, Enzyme Activation, Gene Expression Regulation, Humans, Inflammation, Muscle Contraction, Oxidation-Reduction, Stress, Physiological, Signal Transduction, Exercise, NF-kappa B, Oxidative Stress, Muscle, Skeletal, Mitogen-Activated Protein Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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