Fig. 1

SASP secreted by senescent cells accelerates senescence of surrounding cells. Cytokines such as IL-6 and IL-8 in SASP can act on senescent cells themselves in the form of autocrine, while many other SASP molecules are transmitted from cell to cell in a paracrine form to cause senescence in the neighboring cells, thus exacerbating the pro-senescence effect. p53, p21, p15, and p16 are increased in the pre-senescent cells. On the other hand, the increase of Bcl-XL in the pre-senescence cells enhances their anti-apoptotic ability, which renders the cells undergo senescence instead of apoptosis. Senescent cells within the joint accelerate the progression of OA. IL, Interleukin; SASP, senescence-associated secretory phenotype; GM-CSF, granulocyte macrophage-colony stimulating factor; GRO, growth-regulated oncogene; IGFBP, insulin-like growth factor-binding protein; MMP, matrix metalloproteinase; OA, osteoarthritis