Yugang Tu

TL;DR: This is the first report to demonstrate that UII is increased in diabetes-associated atherosclerosis in humans and rodents and UII receptor antagonism in diabetic Apoe KO mice significantly attenuated diabetes- associated Atherosclerosis and aortic staining.

TL;DR: CDA1 is a potential target for attenuating vascular ECM accumulation caused by enhanced TGF-β action, as seen in diabetic atherosclerosis, through Knockdown of CDA1-encoding gene Tspyl2, which blocked the profibrotic effect of T GF-β in VSMCs.

TL;DR: In vitro and in vivo findings show that CDA1 has a critical role in TGF-β signaling in the kidney, and the Smad3 inhibitor, SIS3, markedly attenuated the activities of Cda1 in stimulating TGF -β signaling as well as gene expression of collagens I, III, and IV.

TL;DR: Investigation of the genetic deletion of Tspyl2 in C57BL6 and ApoE knockout mice suggests that CDA1 deletion reduces but does not block renal TGF-β signaling, which may be a potential therapeutic target for retarding DN and perhaps, other kidney diseases associated with T GF-β-mediated fibrogenesis.

TL;DR: Evidence is provided that CDA1 plays a role in diabetes to reduce susceptibility to aneurysm formation and upregulation of vascular CDA2 is downregulated within biopsies from human abdominal aortic aneurYSms.