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. 2018 Jun 25;9:706. doi: 10.3389/fphys.2018.00706

Figure 2.

Figure 2

Schematic diagram illustrating the interrelation between autophagy, senescence and inflammation in the onset of osteoarthritis (OA). During aging, after trauma or stress associated with to decreased autophagy and increased oxidative stress, chondrocytes become senescent and secrete a Senescence-Associated Secretory Phenotype (SASP). Factors secreted in the SASP propagate senescence and inflammation to surrounding cells and tissues through a paracrine process and participate to OA. Moreover, the cartilage degradation products called damage associated molecular patterns (DAMP) reinforce inflammation and senescence notably via an increase in oxidative stress (ROS). ROS, Reactive oxygen Species; SIRT, Sirtuin; SASP, senescence associated secretory phenotype; NF-kB, nuclear factor-kappa B; cGAS, Cyclic GMP-AMP synthase; STING, stimulator of interferon genes; TLR, Toll-like Receptor; RAGE, Receptor for Advanced-Glycation End Products; HMGB-1, High Mobility group Box-1; IL-1, interleukin-1; TNF, tumor necrosis factor; IL6, interleukin 6; IL8, interleukin 8; DAMP, Damage-Associated molecular pattern.