Figure 4
From: Reaction-Diffusion-Delay Model for EPO/TNF-α Interaction in articular cartilage lesion abatement
Signaling involved in cartilage injury response. The occurrence of an injury begins a sequence of chemical productions that promote the inflammatory response. Lysing (necrotic) cells give off DAMPs (M) resulting in a population of catabolic cells that produce TNF-α (F) and ROS (R). ROS promotes production of EPO (P) by healthy cells while TNF-α acts to block EPO signaling. Furthermore, TNF-α influences degradation of extracellular matrix providing another source of DAMPs. The cells switch state according to the signaling by chemicals produced in response to injury and inflammation. DAMPs and TNF-α drive the C → S T transition, TNF-α drives the S T → S A transition, while TNF-α and DAMPs drive the S T → D A transition. Finally, EPO drives the S A → C transition. This figure illustrates the assumptions of the mathematical model (equations (3-11)). Not shown: DAMPs given off as a result of matrix degradation also influences the switch from healthy to catabolic.