Because the control mechanism of autophagy can remove accumulated proteins in cells,
this avoids the toxic effects of abnormal proteins;
in fact, when neuronal cells or myocardium lose their autophagy function,
ubiquitinated proteins (ubiquitinated proteins) and inclusions are formed.
The accumulation of inclusion bodies, which cannot be diluted by cell division,
can lead to neurodegeneration and cardiac hypertrophy.
Autophagy will decrease with age, and the risk of osteoarthritis also increases with age.
Studies on articular cartilage in humans and experimental mice have shown that the proteins involved in autophagy decrease with age.
Autophagy is continuously activated in normal cartilage and has a chondroprotective effect.
However, autophagy is damaged with age and can cause chondrocyte death and joint structural damage.
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