Overexpression of dimethylarginine dimethylaminohydrolase 1 protects from angiotensin II-induced cardiac hypertrophy and vascular remodeling
Irakli Kopaliani, Natalia Jarzebska, Silke Billoff, Anne Kolouschek, Jens Martens‐Lobenhoffer, Stefan R. Bornstein, Stefanie M. Bode‐Böger, Vinitha N. Ragavan, Norbert Weiss, Arduino A. Mangoni, Andreas Deußen, Roman N. Rodionov
Abstract
We showed that overexpression of dimethylarginine dimethylaminohydrolase 1 (DDAH1) protects from angiotensin II-induced cardiovascular damage, progression of hypertension, and adverse vascular remodeling in vivo. This protective effect is associated with decreased levels of asymmetric dimethylarginine, preservation of endothelial function, inhibition of cardiovascular inflammation, and lower activity of matrix metalloproteinase-2. Our findings are highly clinically relevant, because they suggest that upregulation of DDAH1 might be a promising therapeutic approach against angiotensin II-induced end organ damage.