Figure 3.

Senescence-associated cell transition and interaction (SACTAI) showing the relationship among SomC, MSC, and SnMSC. Due to aging-induced stress, MSCs proliferate and differentiate while SomCs de-differentiate and result in MSC-like cells for tissue repair. Repeated activation of MSC’s replication induces replicative senescence, resulting in SnMSCs. SnMSCs synthesize pro-inflammatory SASPs, which in turns act on SomCs to trigger catabolism and SomC death. Feedback of SomC with TGF-b reinforces the SnMSC properties including inflammation, fibrosis and abnormal calcification.