1. Fig. 2. Potential mechanisms and effects of impaired Ca2+ handling in DC. Impairment in cardiomyocyte Ca2+ influx and efflux, impaired release and reuptake of Ca2+ by the SR, and impaired Ca2+ uptake by the mitochondria which may subsequently impair ATP regeneration and thereby contribute to systolic and diastolic dysfunction in DC.DC, diabetic cardiomyopathy; SR, sarcoplasmic reticulum; ATP, adenosine triphosphate; NCX, Na+/Ca2+ exchanger; LTCC, L-type Ca2+ channels; TCA, trichloroacetic acid; DH, dehydrogenase; RyR, ryanodine receptor; CaMKII, calmodulin-dependent protein kinase II; O-GlcNAc, O-linked β-N-acetylglucosamine; SERCA, sarco(endo)plasmic reticulum Ca2+-ATPase; AGE, advanced glycation end product.
Fig. 2. Potential mechanisms and effects of impaired Ca2+ handling in DC. Impairment in cardiomyocyte Ca2+ influx and efflux, impaired release and reuptake of Ca2+ by the SR, and impaired Ca2+ uptake by the mitochondria which may subsequently impair ATP regeneration and…
J Lipid Atheroscler May;8(1):