Cytokines in aging and muscle homeostasis

J. G. Cannon

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Cytokines are best known as mediators of host defense responses to infection and other environmental stresses. However, some of these proteins (interleukin-1 and tumor necrosis factor) may modulate clearance and repair processes in skeletal muscle following injury, and others (fibroblast growth factor and platelet-derived growth factor) may be involved with the sustained viability of muscle cells. Muscle repair and vitality also require neuronal contact (influenced by nerve growth factor and ciliary neurotrophic factor) as well as angiogenesis and connective tissue matrix formation (influenced by transforming growth factor β). Successful muscle aging will depend in part on how well a muscle repairs itself after damage. This includes not only overt injury, but also the daily 'wear and tear' that may not be perceived via pain or alterations in function. Age-related loss of muscle mass or function may be the cumulative result of repeated episodes of incomplete repair. Abnormal production or sensitivity to cytokines by aged cells may contribute to these changes in muscle mass and function.

Original languageEnglish (US)
Pages (from-to)120-123
Number of pages4
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume50
Issue numberSPEC. ISSUE
StatePublished - Jan 1 1995

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Homeostasis
Cytokines
Muscles
Ciliary Neurotrophic Factor
Fibroblast Growth Factors
Platelet-Derived Growth Factor
Wounds and Injuries
Transforming Growth Factors
Nerve Growth Factor
Tears
Interleukin-1
Connective Tissue
Muscle Cells
Skeletal Muscle
Tumor Necrosis Factor-alpha
Pain
Infection
Proteins

ASJC Scopus subject areas

  • Aging

Cite this

Cytokines in aging and muscle homeostasis. / Cannon, J. G.

In: Journals of Gerontology - Series A Biological Sciences and Medical Sciences, Vol. 50, No. SPEC. ISSUE, 01.01.1995, p. 120-123.

Research output: Contribution to journalArticle

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