Oxidative stress and fibrosis in incipient myocardial dysfunction in type 2 diabetic patients

Coenzyme Q10 attenuates diastolic dysfunction, cardiomyocyte hypertrophy and cardiac fibrosis in the db/db mouse model of type 2 diabetes

“…Interestingly in the current study, ramipril failed to reduce systemic lipid peroxidation, but it effectively lowered cardiac superoxide production, as previously described [39,40]. The reduced generation of ROS (and hence restored redox balance) achieved by coenzyme Q 10 and ramipril treatment in the present study is likely to be a key mechanism by which they limited myocardial fibrosis and cardiomyocyte hypertrophy in this model of type 2 diabetes, as has been implicated in other settings of cardiac fibrosis [25,41] and LV hypertrophy [22,42,43].…”

“…Hyperglycaemia-induced ROS generation has been implicated as a key stimulator of these cardiac impairments [25,26]. Consequently, reducing oxidative stress, in particular excess cardiac superoxide generation, should be favourable in the management of diabetic cardiomyopathy.…”

Serum carboxy-terminal propeptide of type I procollagen (PIP) is a marker of diastolic dysfunction in patients with early type 2 diabetes mellitus

“…Recently, Gonzalez-Vilchez et al reported a correlation between serum marker of myocardial fibrosis and standard parameter of systolic function in T2DM patients [12]. But our results and participants were different from the study of GonzalezVilchez et al [12] in that we showed a correlation between serum PIP and parameter of LV diastolic dysfunction in patients with early T2DM and excluded LVH and hypoglycemic agents controlled diabetic patients.…”

Cardiac impairment in rabbits fed a high-fat diet is counteracted by dehydroepiandrosterone supplementation

“…We believe that DHEA's key action is against oxidative imbalance (Brignardello et al 2007;Aragno et al 2006), which could be critical in inducing myocardial dysfunction. A greater propensity for oxidative stress after myocardial infarction is associated with the development of heart failure (Smith et al 2005) and a correlation between systolic and diastolic myocardial dysfunction and oxidative stress has been reported in a highly-selected group of uncomplicated type 2 diabetic patients (González-Vílchez et al 2005). Here we show that increased H 2 O 2 , increased end-products of lipid peroxidation (specifically HNE) and increased activation of the transcription factor p65-NFkB in the cardiac tissue of HF rabbits, are all counteracted by DHEA.…”