Prashanti Patil1, Laura J Niedernhofer2, Paul D Robbins2, Joon Lee1, Gwendolyn Sowa1,3, Nam Vo1. 1. Department of Orthopedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA. 2. Institute on the Biology of Aging and Metabolism, Department of Biochemistry, Molecular Biology and Biophysics, University of Minnesota Medical School, Minneapolis, MN. 3. Department of Orthopedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA. Department of Physical Medicine and Rehabilitation, University of Pittsburgh, Pittsburgh, PA, USA.
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.
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.
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