Reduced hybrid/complex N-glycosylation disrupts cardiac electrical signaling and calcium handling in a model of dilated cardiomyopathy
Dilated cardiomyopathy (DCM) is the third most common cause of heart failure, with ~70% of DCM cases considered idiopathic. We showed recently, through genetic ablation of the MGAT1 gene, which encodes an essential glycosyltransferase (GlcNAcT1), that prevention of cardiomyocyte hybrid/complex N-glycosylation was sufficient to cause DCM that led to heart failure and early death. Our findings are consistent with increasing evidence suggesting a link between aberrant glycosylation and heart diseases of acquired and congenital etiologies.
Source: Journal of Molecular and Cellular Cardiology - Category: Cytology Authors: Andrew R. Ednie, Austin R. Parrish, Martha J. Sonner, Eric S. Bennett Source Type: research
More News: Calcium | Cardiology | Cardiomyopathy | Cytology | Dilated Cardiomyopathy | Genetics | Heart | Heart Failure