Table 1 Telomeres and oxidative stress contribute to cellular senescence also related to OA

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

[34, 35]

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]