Factors | Correlation with senescence | Refs | Correlation with OA | Refs |
---|---|---|---|---|
Telomeres | DNA repair mechanisms recognized telomere shortening triggers the DNA damage response leading to senescence | [23] | Negative associations of oxidative stress and inflammatory factors levels with RTL in the knee joints of OA patients | [29] |
Cells lacking telomerase trigger the DNA damage response leading to senescence | [25] | Shorter TL in OA patients | [24] | |
Oxidative stress accelerates cellular senescence by shortening telomeres | [27] | |||
Inflammation can lead to telomere abrasion inducing cellular senescence | [28] | |||
Oxidative stress | ROS accumulation, cell cycle arrest and cellular senescence accompanied by upregulation of p53 and p21 proteins in cells | [31] | Increased levels of intracellular ROS disrupt cartilage homeostasis and lead to cartilage damage in OA | [39] |
Cellular senescence is largely dependent on ROS | Intracellular ROS level were elevated in posttraumatic OA | [20] | ||
ROS induced premature senescence by PI3K/Akt/mTOR pathway | [33] | The production of intracellular superoxide is increased in OA patients | [38] |