Cellular senescence in intervertebral disc aging and degeneration.

Authors:
Prashanti Patil
Prashanti Patil
University of Pittsburgh
Pittsburgh | United States
Laura J Niedernhofer
Laura J Niedernhofer
University of Pittsburgh School of Medicine
United States
Paul D Robbins
Paul D Robbins
University of Pittsburgh School of Medicine
United States
Joon Lee
Joon Lee
Sungkyunkwan University School of Medicine
South Korea
Gwendolyn Sowa
Gwendolyn Sowa
University of Pittsburgh
Quezon City | Philippines
Mr. Nam Vo
Mr. Nam Vo
Ho Chi Minh, Ho Chi Minh City | Vietnam

Curr Mol Biol Rep 2018 Dec 25;4(4):180-190. Epub 2018 Oct 25.

Department of Orthopedic Surgery, University of Pittsburgh, Pittsburgh, PA, USA.

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, 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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Source
http://link.springer.com/10.1007/s40610-018-0108-8
Publisher Site
http://dx.doi.org/10.1007/s40610-018-0108-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6248341PMC

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December 2018
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