The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Autophagy activation by rapamycin reduces severity of experimental osteoarthritis
Open accessAbstract
Objectives Osteoarthritis is associated with cell death and extracellular matrix degradation in articular cartilage. Autophagy is an essential cellular homeostasis mechanism that was found to be deficient in ageing and osteoarthritic cartilage. This study determined whether pharmacological inhibition of the mammalian target of rapamycin (mTOR), a key inhibitor of autophagy, has disease-modifying activity in experimental osteoarthritis. Methods Experimental osteoarthritis was induced by transection of the medial meniscotibial ligament and the medial collateral ligament in 2-month-old C57Bl/6 mice (n=36). Rapamycin (1 mg/kg weight/day) (n=18 mice) or dimethyl sulphoxide vehicle control (n=18 mice) was administered intraperitoneally for 10 weeks. Histopathological changes in articular cartilage and synovium were examined by using semiquantitative scoring systems. Rapamycin effects on mTOR signalling, autophagy, cartilage homeostasis and inflammation were analysed by immunohistochemistry and immunofluorescence staining. Results Rapamycin affected the mTOR signalling pathway in mouse knee joints as indicated by the inhibition of ribosomal protein S6 phosphorylation, a target of mTOR and activation of LC3, a main marker of autophagy. The severity of cartilage degradation was significantly (p<0.01) reduced in the rapamycin-treated group compared with the control group and this was associated with a significant (p<0.05) decrease in synovitis. Rapamycin treatment also maintained cartilage cellularity and decreased ADAMTS-5 and interleukin-1β expression in articular cartilage. Conclusions These results suggest that rapamycin, at least in part by autophagy activation, reduces the severity of experimental osteoarthritis. Pharmacological activation of autophagy may be an effective therapeutic approach for osteoarthritis.
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Cites
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Cited by
Osteoarthritis: pathogenic signaling pathways and therapeutic targets
Yao, Q., Wu, X., Tao, C., Gong, W., Chen, M., Qu, M., Zhong, Y., He, T., Chen, S., & Xiao, G. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01330-w · Cited by 1,194
Mechanisms and therapeutic implications of cellular senescence in osteoarthritis
Coryell, P. R., Diekman, B. O., & Loeser, R. F. (2021) · Nature Reviews Rheumatology · doi:10.1038/s41584-020-00533-7 · Cited by 761
The role of metabolism in the pathogenesis of osteoarthritis
Mobasheri, A., Rayman, M. P., Gualillo, O., Sellam, J., van der Kraan, P., & Fearon, U. (2017) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2017.50 · Cited by 742
Effects of aging on articular cartilage homeostasis
Lotz, M., & Loeser, R. F. (2012) · Bone · doi:10.1016/j.bone.2012.03.023 · Cited by 398
Self-citationChen, X., Gong, W., Shao, X., Shi, T., Zhang, L., Dong, J., Shi, Y., Shen, S., Qin, J., Jiang, Q., et al. (2022) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2021-221091 · Cited by 359
Metadata
- Authors
- Caramés, B., Hasegawa, A., Taniguchi, N., Miyaki, S., Blanco, F. J., & Lotz, M.
- Venue
- Annals of the Rheumatic Diseases
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 71
- Issue
- 4
- Pages
- 575-581
- ISSN
- 0003-4967 (ISSN-L)
- OpenAlex
- W2108888253
- Cited by
- 455
- References
- 43
- FWCI
- 8.95
- Type
- journal article
- Language
- en
- Open access
- green
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