Table 4.

Pro-fibrotic roles of GSK-3β in various organs/tissues.

Models	Organs/Tissues	Outcomes	References
Male Wistar rats	Heart	Inhibited GSK-3β activity significantly ameliorated cardiac collagen deposition, thereby preventing the development of cardiac fibrosis in diabetic rats.	112
Metallothionein -overexpressing transgenic mice	Heart	Inactivation of GSK-3β significantly represses diabetes-induced cardiac fibrosis by reducing collagen deposition and inflammation.	113
Arrb2 KO mice	Liver	GSK-3β inactivation improves hepatic fibrosis by reducing hepatocyte apoptosis and hepatic injury.	116
C57BL/6 mice	Kidney	Following I/R, GSK-3β increasesα-SMA expression, COLLΙ and FN deposition, and macrophage infiltration.	117
Arrb2 KO mice	Kidney	Activation of GSK-3β increases COLLΙ and FN deposition as well as α-SMA expression, thereby aggravating bilateral IR-induced renal fibrosis.	118
Human lung fibroblasts	Lung	GSK-3β inhibition prevents α-SMA and FN expression, inflammation, and ECM production, and may be beneficial in pulmonary fibrosis.	120
C57BL/6 mice	Lung	Down-regulation of GSK-3β can reverse established mesothelial mesenchymal transition and improve lung function. However, increased GSK-3β expression colocalized with the increased expression of α-SMA and COLLΙ.	121