Cellular senescence in intervertebral disc aging and degeneration
- PMID: 30473991
- PMCID: PMC6248341
- DOI: 10.1007/s40610-018-0108-8
Cellular senescence in intervertebral disc aging and degeneration
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.
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.
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