Table 1.

YAP Involves the Regulation of Pathophysiological Process in RA

Signaling	Cell Types	Main Results	Reference
TGF-β signaling	Fibroblast-like synoviocytes (FLSs)	FLSs displayed overexpression of PTPN14 and YAP, PTPN14 combined with YAP increased the nuclear location YAP, promoted the TGF-β-dependent SMAD3 nuclear localization. Inhibition of YAP reduced FLSs pathogenic phenotype and ameliorated arthritis severity.	Angel Bottini, et al72
YAP-Akt signaling	Human umbilical vein endothelial cells	YAP expression and nuclear translocation were increased in umbilical vein endothelial cells. Increased YAP expression contributed the angiogenesis of the synovial tissue patients of RA. The YAP interacted with the PI3K/Akt pathway regulated the proliferation and invasion of cells, pathogenic progress of RA.	Qiyue Chen, et al71
YAP/TAZ signaling	Fibroblast-like synoviocytes (FLSs)	YAP/TAZ transcriptional activity was increased in RA FLSs. Increased YAP/TAZ transcriptional activity induced a common phenotype in RA FLSs with an elevated in apoptosis, proliferation, invasion, and inflammatory response.	Robin Caire, et al67
IL-6–YAP–Snail signaling	Synovial fibroblasts	YAP was upregulated in hyperplastic human RA synovial fibroblasts and mouse synovium. Increased expression of YAP showed an erosive phenotype, invading cartilage and bone in RA, IL-6 activates YAP through Jak and induces YAP–Snail interaction in SF to promote the invasiveness activity and inflammatory response in RA.	Rebecca A Symons, et al70
YAP/TAZ signaling	Fibroblast Synovial Cells (FLSs)	YAP and TAZ were upregulated in RA-FLSs, knockdown of YAP or TAZ inhibited the migration and invasion of FLSs, ameliorated arthritis severity. The suppression of YAP/TAZ signaling pathway promoted the activity of autophagy implied by the accumulation of LC3B-II and ULK1. YAP/TAZ and autophagy play important roles in the migration and invasion of RA-FLSs.	Wei Zhou, et al74