Molecular basis of high glucose-mediated cardiac calcium mishandling

ConclusionOur data suggests that HG alters Ca2 +  signalling via Epac2–mediated pro-arrhythmic events due a CaMKII-dependent increase of RyR2 activity. Overtime, this newly described mechanism lowers systolic Ca2 +  release as seen in diabetic-associated cardiomyopathy.
Source: Archives of Cardiovascular Diseases Supplements - Category: Cardiology Source Type: research