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
. 2024 Oct 8;25(19):10805.
doi: 10.3390/ijms251910805.

TNFα-Related Chondrocyte Inflammation Models: A Systematic Review

Su Wang  1 , Sarah Kurth  1 , Christof Burger  1 , Dieter C Wirtz  1 , Frank A Schildberg  1 , Robert Ossendorff  1
Affiliations

TNFα-Related Chondrocyte Inflammation Models: A Systematic Review

Su Wang et al. Int J Mol Sci. .

Abstract

Tumor necrosis factor alpha (TNFα), as a key pro-inflammatory cytokine, plays a central role in joint diseases. In recent years, numerous models of TNFα-induced cartilage inflammation have been developed. However, due to the significant differences between these models and the lack of consensus in their construction, it becomes difficult to compare the results of different studies. Therefore, we summarized and compared these models based on important parameters for model construction, such as cell source, cytokine concentration, stimulation time, mechanical stimulation, and more. We attempted to analyze the advantages and disadvantages of each model and provide a compilation of the analytical methods used in previous studies. Currently, TNFα chondrocyte inflammation models can be categorized into four main types: monolayer-based, construct-based, explant-based TNFα chondrocyte inflammation models, and miscellaneous TNFα chondrocyte inflammation models. The most commonly used models were the monolayer-based TNFα chondrocyte inflammation models (42.86% of cases), with 10 ng/mL TNFα being the most frequently used concentration. The most frequently used chondrocyte cell passage is passage 1 (50%). Human tissues were most frequently used in experiments (51.43%). Only five articles included models with mechanical stimulations. We observed variations in design conditions between different models. This systematic review provides the essential experimental characteristics of the available chondrocyte inflammation models with TNFα, and it provides a platform for better comparison between existing and new studies in this field. It is essential to perform further experiments to standardize each model and to find the most appropriate experimental parameters.

Keywords: TNFα; cartilage; chondrocyte; cytokine; inflammation model.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Figures

Figure 1
Figure 1
Identification and selection of studies via databases and registers.
Figure 2
Figure 2
Summary of TNFα chondrocyte inflammation models.
Figure 3
Figure 3
Concentration of TNFα in ng/mL used in different models (a): monolayer-based TNFα chondrocyte inflammation models, (b): construct-based TNFα chondrocyte inflammation models, and (c) explant-based TNFα chondrocyte inflammation models.
Figure 4
Figure 4
Summary of TNFα stimulation durations in hours and/or days (a): monolayer-based models, (b): construct-based models, and (c): explant-based models.
Figure 5
Figure 5
Passages’ (P0–P3) distribution of chondrocytes TNFα inflammation models.
Figure 6
Figure 6
Species distribution of TNFα chondrocyte inflammation models.
See this image and copyright information in PMC

Similar articles

See all similar articles

References

    1. Baud V., Karin M. Signal transduction by tumor necrosis factor and its relatives. Trends Cell Biol. 2001;11:372–377. doi: 10.1016/S0962-8924(01)02064-5. - DOI - PubMed
    1. Horiuchi T., Mitoma H., Harashima S.-I., Tsukamoto H., Shimoda T. Transmembrane TNF-alpha: Structure, function and interaction with anti-TNF agents. Rheumatology. 2010;49:1215–1228. doi: 10.1093/rheumatology/keq031. - DOI - PMC - PubMed
    1. Jiang Y., Yu M., Hu X., Han L., Yang K., Ba H., Zhang Z., Yin B., Yang X.-P., Li Z., et al. STAT1 mediates transmembrane TNF-alpha-induced formation of death-inducing signaling complex and apoptotic signaling via TNFR1. Cell Death Differ. 2017;24:660–671. doi: 10.1038/cdd.2016.162. - DOI - PMC - PubMed
    1. Bradley J.R. TNF-mediated inflammatory disease. J. Pathol. 2008;214:149–160. doi: 10.1002/path.2287. - DOI - PubMed
    1. Jang D.-I., Lee A.-H., Shin H.-Y., Song H.-R., Park J.-H., Kang T.-B., Lee S.-R., Yang S.-H. The Role of Tumor Necrosis Factor Alpha (TNF-α) in Autoimmune Disease and Current TNF-α Inhibitors in Therapeutics. Int. J. Mol. Sci. 2021;22:2719. doi: 10.3390/ijms22052719. - DOI - PMC - PubMed

Publication types

Substances

LinkOut - more resources