Skeletal Muscle as Potential Central Link between Sarcopenia and Immune Senescence
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As our population grows older, age-related pathologies are becoming more prevalent. Deterioration of skeletal muscle and the immune system manifests as sarcopenia and immune senescence respectively. The disease burden of these pathologies emphasizes the need for a better understanding of the underlying mechanisms. Skeletal muscle has emerged as a potent regulator of immune system function. As such, skeletal muscle might be the central integrator between sarcopenia and immune senescence in an aging biological system. Therapeutic approaches targeting skeletal muscle might be able to restore both muscle and immune system function. In this review, we therefore outline the current - however still fragmentary - knowledge about the potential communication pathways of muscle and immune system, how they are affected by aging of skeletal muscle and discuss possible treatment strategies. The review intends to be hypothesis-generating and should thereby stimulate further research in this important scientific field.
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Chronic, low-grade inflammation induces muscle catabolism via pleiotropic mechanisms mediated by the inflammatory secretome, whereas acute inflammation activates anabolic pathways leading to muscle regeneration.
“Chronic, low-grade inflammation induces muscle catabolism via pleiotropic mechanisms mediated by the inflammatory secretome [20], whereas acute inflammation (exercise-mediated or in acute muscle injury models) activates anabolic pathways leading to muscle regeneration.”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [20]
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- Authors
- Nelke, C., Dziewas, R., Minnerup, J., Meuth, S. G., & Ruck, T.
- Affiliations
- University of Münster (DE)
- Corresponding author
- Ruck, Tobias
- Venue
- eBioMedicine
- Publisher
- Elsevier BV
- Published
- 2019-11
- Volume
- 49
- Pages
- 381-388
- ISSN
- 2352-3964 (ISSN-L)
- PMC
- PMC6945275
- OpenAlex
- W2981890331
- Cited by
- 437
- References
- 76
- Citations by year
- 2026: 61 · 2025: 68 · 2024: 67 · 2023: 74 · 2022: 90 · 2021: 46 · 2020: 30 · 2018: 1
- FWCI
- 4.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- EBioMedicine (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Innovative Medizinische Forschung (IMF) Münster (I-RU211405, I-RU211811)
- Else-Kröner-Fresenius-Stiftung (2018_A03)
- German Research Foundation (2169/2-1)
- Topics
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- sarcopenia, immunosenescence, skeletal muscle, aging, muscle atrophy, treatment options, muscle function
- MeSH terms
- Aging, Cell Communication, Humans, Immune System, Risk Factors, Muscle, Skeletal, Sarcopenia
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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