Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Dec;4(4):180-190.
doi: 10.1007/s40610-018-0108-8. Epub 2018 Oct 25.

Cellular senescence in intervertebral disc aging and degeneration

Prashanti Patil  1 , Laura J Niedernhofer  2 , Paul D Robbins  2 , Joon Lee  1 , Gwendolyn Sowa  1   3 , Nam Vo  1
Affiliations

Cellular senescence in intervertebral disc aging and degeneration

Prashanti Patil et al. Curr Mol Biol Rep. 2018 Dec.

Abstract

Purpose: Age is a major risk factor for multiple disease pathologies, including chronic back pain, which stems from age-related degenerative changes to intervertebral disc tissue. Growing evidence suggest that the change in phenotype of disc cells to a senescent phenotype may be one of the major driving forces of age-associated disc degeneration. This review discusses the known stressors that promote development of senescence in disc tissue and the underlying molecular mechanisms disc cells adopt to enable their transition to a senescent phenotype.

Recent findings: Increased number of senescent cells have been observed with advancing age and degeneration in disc tissue. Additionally, in vitro studies have confirmed the catabolic nature of stress-induced senescent disc cells. Several factors have been shown to establish senescence via multiple different underlying mechanisms.

Summary: Cellular senescence can serve as a therapeutic target to combat age-associated disc degeneration. However, whether the different stressors utilizing different signaling networks establish different kinds of senescent types in disc cells is currently unknown and warrants further investigation.

Keywords: Aging; cellular senescence; intervertebral disc degeneration.

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest Prashanti Patil, Joon Lee, Gwendolyn Sowa, and Nam Vo each declare no potential conflicts of interest. Laura J. Niedernhofer is an SAB member for Innate Biologics and Castle Creek, and reports a patent pending. Paul D. Robbins is an SAB member for Innate Biologics, Tissuegene, Unicyte, Engene, and Genascence and co-founder of Genascence. Dr. Robbins also reports a patent pending.

References

    1. Acharyya S, et al. Interplay of IKK/NF-kappaB signaling in macrophages and myofibers promotes muscle degeneration in Duchenne muscular dystrophy. J Clin Invest. 2007;117:889–901. - PMC - PubMed
    1. Adler AS, et al. Motif module map reveals enforcement of aging by continual NF-kappaB activity. Genes Dev. 2007;21:3244–57. - PMC - PubMed
    1. Antoniou J, Steffen T, Nelson F, Winterbottom N, Hollander A, Poole R, Aebi M, and Alini M. The human lumbar intervertebral disc: evidence for changes in the biosynthesis and denaturation of the extracellular matrix with growth, maturation, ageing, and degeneration. J. Clin. Invest 1996; 98(4): 996–1003 - PMC - PubMed
    1. Bachmeier BE, et al. Analysis of tissue distribution of TNF-alpha, TNF-alpha-receptors, and the activating TNF-alpha-converting enzyme suggests activation of the TNF-alpha system in the aging intervertebral disc. Ann N Y Acad Sci. 2007;1096:44–54. - PubMed
    1. Bachmeier BE, Nerlich AG, Weiler C, Paesold G, Jochum M, Boos N. Analysis of tissue distribution of TNF-alpha, TNF-alpha-receptors, and the activating TNF-alpha-converting enzyme suggests activation of the TNF-alpha system in the aging intervertebral disc. Ann N Y Acad Sci. 2007;1096:44–54. - PubMed

LinkOut - more resources