The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
STING promotes senescence, apoptosis, and extracellular matrix degradation in osteoarthritis via the NF-κB signaling pathway
Open accessAbstract
Damaged deoxyribonucleic acid (DNA) is a primary pathologic factor for osteoarthritis (OA); however, the mechanism by which DNA damage drives OA is unclear. Previous research demonstrated that the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) participates in DNA damage response. As a result, the current study aimed at exploring the role STING, which is the major effector in the cGAS-STING signaling casacde, in OA progress in vitro, as well as in vivo. In this study, the expression of STING was evaluated in the human and mouse OA tissues, and in chondrocytes exposed to interleukin-1 beta (IL-1β). The influences of STING on the metabolism of the extracellular matrix (ECM), apoptosis, and senescence, were assessed in STING overexpressing and knocking-down chondrocytes. Moreover, the NF-κB-signaling casacde and its role in the regulatory effects of STING on ECM metabolism, apoptosis, and senescence were explored. The STING knockdown lentivirus was intra-articularly injected to evaluate its therapeutic impact on OA in mice in vivo. The results showed that the expression of STING was remarkably elevated in the human and mouse OA tissues and in chondrocytes exposed to IL-1β. Overexpression of STING promoted the expression of MMP13, as well as ADAMTS5, but suppressed the expression of Aggrecan, as well as Collagen II; it also enhanced apoptosis and senescence in chondrocytes exposed to and those untreated with IL-1β. The mechanistic study showed that STING activated NF-κB signaling cascade, whereas the blockage of NF-κB signaling attenuated STING-induced apoptosis and senescence, and ameliorated STING-induced ECM metabolism imbalance. In in vivo study, it was demonstrated that STING knockdown alleviated destabilization of the medial meniscus-induced OA development in mice. In conclusion, STING promotes OA by activating the NF-κB signaling cascade, whereas suppression of STING may provide a novel approach for OA therapy.
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Cites
1 retracted
Park, C., Jeong, J.-W., Lee, D.-S., Yim, M., Lee, J., Han, M. H., Kim, S., Kim, H., Kim, G., Park, E. K., et al. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19082308 · Cited by 67
RetractedMolecular mechanisms and cellular functions of cGAS–STING signalling
Hopfner, K.-P., & Hornung, V. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0244-x · Cited by 2,052
Kraus, V. B., Huebner, J. L., DeGroot, J., & Bendele, A. (2010) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2010.04.015 · Cited by 1,771
Glasson, S. S., Blanchet, T. J., & Morris, E. A. (2007) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2007.03.006 · Cited by 1,514
Blagojevic, M., Jinks, C., Jeffery, A., & Jordan, K. P. (2010) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2009.08.010 · Cited by 1,397
Cytoplasmic chromatin triggers inflammation in senescence and cancer
Dou, Z., Ghosh, K., Vizioli, M. G., Zhu, J., Sen, P., Wangensteen, K. J., Simithy, J., Lan, Y., Lin, Y., Zhou, Z., et al. (2017) · Nature · doi:10.1038/nature24050 · Cited by 1,335
Self-citationThe Cytosolic DNA-Sensing cGAS–STING Pathway in Cancer
Kwon, J., & Bakhoum, S. F. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0761 · Cited by 1,293
Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence
Glück, S., Guey, B., Gulen, M. F., Wolter, K., Kang, T.-W., Schmacke, N. A., Bridgeman, A., Rehwinkel, J., Zender, L., & Ablasser, A. (2017) · Nature Cell Biology · doi:10.1038/ncb3586 · Cited by 1,196
Targeting STING with covalent small-molecule inhibitors
Haag, S. M., Gulen, M. F., Reymond, L., Gibelin, A., Abrami, L., Decout, A., Heymann, M., van der Goot, F. G., Turcatti, G., Behrendt, R., et al. (2018) · Nature · doi:10.1038/s41586-018-0287-8 · Cited by 1,178
cGAS is essential for cellular senescence
Yang, H., Wang, H., Ren, J., Chen, Q., & Chen, Z. J. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1705499114 · Cited by 1,009
Cited by
Jiang, S.-Y., Tian, T., Yao, H., Xia, X.-M., Wang, C., Cao, L., Hu, G., Du, R.-H., & Lu, M. (2023) · Cell Death & Differentiation · doi:10.1038/s41418-023-01216-y · Cited by 123
Trans-Golgi network tethering factors regulate TBK1 trafficking and promote the STING-IFN-I pathway
Wang, J., Niu, S., Hu, X., Li, T., Liu, S., Tu, Y., Shang, Z., Zhao, L., Xu, P., Lin, J., et al. (2025) · Cell Discovery · doi:10.1038/s41421-024-00763-z · Cited by 30
Ren, P., Zheng, C., Pang, Y., Qiang, Y., Sun, S., Wang, Q., Xu, W., Lee, M., Lu, Z., Zhou, M., et al. (2025) · Nature Aging · doi:10.1038/s43587-025-01011-z · Cited by 6
Metadata
- Authors
- Guo, Q., Chen, X., Chen, J., Zheng, G., Xie, C., Wu, H., Miao, Z., Lin, Y., Wang, X., Gao, W., Zheng, X., Pan, Z., Zhou, Y., Wu, Y., & Zhang, X.
- Venue
- Cell Death & Disease
- Published
- 2021-01-04
- Volume
- 12
- Issue
- 1
- Pages
- 13-13
- ISSN
- 2041-4889 (ISSN-L)
- OpenAlex
- W3120339302
- Cited by
- 253
- References
- 46
- FWCI
- 22.80
- Type
- journal article
- Language
- en
- Open access
- gold
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- Guo, Q., Chen, X., Chen, J., Zheng, G., Xie, C., Wu, H., Miao, Z., Lin, Y., Wang, X., Gao, W., Zheng, X., Pan, Z., Zhou, Y., Wu, Y., & Zhang, X. (2021). STING promotes senescence, apoptosis, and extracellular matrix degradation in osteoarthritis via the NF-κB signaling pathway. Cell Death & Disease. https://doi.org/10.1038/s41419-020-03341-9
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