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
Review
. 2020 Mar 29;21(7):2358.
doi: 10.3390/ijms21072358.

The Role of Chondrocyte Hypertrophy and Senescence in Osteoarthritis Initiation and Progression

Yeri Alice Rim  1 , Yoojun Nam  1 , Ji Hyeon Ju  1   2
Affiliations
Review

The Role of Chondrocyte Hypertrophy and Senescence in Osteoarthritis Initiation and Progression

Yeri Alice Rim et al. Int J Mol Sci. .

Abstract

Osteoarthritis (OA) is the most common joint disease that causes pain and disability in the adult population. OA is primarily caused by trauma induced by an external force or by age-related cartilage damage. Chondrocyte hypertrophy or chondrocyte senescence is thought to play a role in the initiation and progression of OA. Although chondrocyte hypertrophy and cell death are both crucial steps during the natural process of endochondral bone formation, the abnormal activation of these two processes after injury or during aging seems to accelerate the progression of OA. However, the exact mechanisms of OA progression and these two processes remain poorly understood. Chondrocyte senescence and hypertrophy during OA share various markers and processes. In this study, we reviewed the changes that occur during chondrocyte hypertrophy or senescence in OA and the attempts that were made to regulate them. Regulation of hypertrophic or senescent chondrocytes might be a potential therapeutic target to slow down or stop OA progression; thus, a better understanding of the processes is required for management.

Keywords: articular cartilage; chondrocyte; hypertrophy; osteoarthritis; senescence.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic image of (a) endochondral ossification in the embryonic cartilage and (b) progression of osteoarthritis in the articular cartilage.
Figure 2
Figure 2
A theoretical model for the relationships of chondrocyte hypertrophy and chondrocyte senescence and the initiation or progression of osteoarthritis (OA). When trauma is induced by mechanical injury or aging, biomechanical stress and oxidative stress increase in the cartilage environment. Increased chondrocyte hypertrophy and senescence induce decreased anabolic signaling and increased catabolic signaling. This results in suppressed glycosaminoglycan (GAG) production by normal chondrocytes and increases the expression of extracellular matrix (ECM)-degrading enzymes and inflammatory cytokines.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Nam Y., Rim Y.A., Jung S.M., Ju J.H. Cord blood cell-derived iPSCs as a new candidate for chondrogenic differentiation and cartilage regeneration. Stem Cell Res. Ther. 2017;8:16. doi: 10.1186/s13287-017-0477-6. - DOI - PMC - PubMed
    1. Rim Y.A., Nam Y., Ju J.H. Application of Cord Blood and Cord Blood-Derived Induced Pluripotent Stem Cells for Cartilage Regeneration. Cell Transpl. 2019;28:529–537. doi: 10.1177/0963689718794864. - DOI - PMC - PubMed
    1. Jeon O.H., David N., Campisi J., Elisseeff J.H. Senescent cells and osteoarthritis: A painful connection. J Clin. Invest. 2018;128:1229–1237. doi: 10.1172/JCI95147. - DOI - PMC - PubMed
    1. Dreier R. Hypertrophic differentiation of chondrocytes in osteoarthritis: The developmental aspect of degenerative joint disorders. Arthritis Res. Ther. 2010;12:216. doi: 10.1186/ar3117. - DOI - PMC - PubMed
    1. Riedl M., Witzmann C., Koch M., Lang S., Kerschbaum M., Baumann F., Krutsch W., Docheva D., Alt V., Pfeifer C. Attenuation of Hypertrophy in Human MSCs via Treatment with a Retinoic Acid Receptor Inverse Agonist. Int. J. Mol. Sci. 2020;21:1444. doi: 10.3390/ijms21041444. - DOI - PMC - PubMed

MeSH terms