Osteoarthritis seems to be an inevitable condition with aging. How would one go about (i) preventing it, and (ii) reversing it?
I haven’t dug into this issue much - but isn’t it believed that exercise is good both in terms of prevention, and in minimizing its progression?
Rapamycin-PLGA microspheres induce autophagy and prevent senescence in chondrocytes and exhibit long in vivo residence
Autophagy, a cellular homeostasis mechanism has a protective role in OA during stress but gets downregulated in OA. Rapamycin, a potent immunomodulator, has shown promise in OA treatment by autophagy activation and is known to prevent senescence. However, its clinical translation for OA is hampered due to systemic toxicity as high and frequent doses are required. Hence, there is a need to develop suitable delivery carriers that can result in sustained and controlled release of the drug in the joint.
Rapamycin, an FDA approved drug in the market for the past 20 years has been shown to prevent OA progression in mice models[17, 18, 25-27]. Rapamycin induces autophagy by inhibiting the mTOR pathway [18, 26]. When mice subjected to the destabilization of the medial menisci (DMM) were treated with rapamycin, a pharmacological activator of autophagy, chondrocyte cellularity was preserved and severe damage and degeneration was prevented in the articular cartilage [17, 18, 27]. Rapamycin is also known to be a senomorphic (senescence prevention) drug which can potentially prevent the cells under stress from turning into senescent phenotypes [28-31]. Thus, rapamycin-induced chondrocyte autophagy and senescence prevention can play a significant role in OA disease modification.
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Intra-articular Injection of Rapamycin Microparticles Prevent Senescence and Effectively Treat Osteoarthritis
https://aiche.onlinelibrary.wiley.com/doi/10.1002/btm2.10298
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Autophagy prevents age-related OA
Autophagy, a mechanism of organelle recycling that promotes cell survival, has been previously implicated in osteoarthritis (OA). One of the proteins fundamental to this process, autophagy protein 5 (Atg5), has now been shown to be protective against late-onset OA in a new study in mice.