Diabetic cardiomyopathy

Acar, Eser; Ural, Dilek; Bildirici, Ulaş; Şahı̇n, Tayfun; Yılmaz, İrem

doi:10.5152/akd.2011.196

Cited by 30 publications

(30 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition to diastolic dysfunction, hyperglycemia can cause modest systolic impairment (22). To determine the extent by which systolic function was impaired in this study, we evaluated EF and FS using echocardiography.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Direct renin inhibition prevents cardiac dysfunction in a diabetic mouse model: comparison with an angiotensin receptor antagonist and angiotensin-converting enzyme inhibitor

et al. 2013

View full text Add to dashboard Cite

Hyperglycemia upregulates intracellular angiotensin II production in cardiac myocytes, effects of which are blocked more effectively by renin inhibition than angiotensin receptor blockers (ARBs) or ACE inhibitors. Here we determined whether renin inhibition is more effective at preventing diabetic cardiomyopathy than an ARB or ACE inhibitor. Diabetes was induced in adult mice for 10 wks by streptozotocin. Diabetic mice were treated with insulin, aliskiren (renin inhibitor), benazeprilat (ACE inhibitor), or valsartan (ARB) via subcutaneous minipumps. Significant impairment in diastolic and systolic cardiac function was observed in diabetic mice, which was completely prevented by all three RAS inhibitors. Hyperglycemia significantly increased cardiac oxidative stress and circulating inflammatory cytokines, which were blocked by aliskiren and benazeprilat, while valsartan was partially effective. Diabetes increased cardiac (pro)renin receptor (PRR) expression and nuclear translocation of promyelocytic zinc finger protein (PLZF), which was completely prevented by aliskiren and valsartan, and partially by benazeprilat. Renin inhibition provided similar protection of cardiac function as ARBs and ACE inhibitors. Activation of PLZF by PRR represented a novel mechanism in diabetic cardiomyopathy. Differential effects of the three agents on oxidative stress, cytokines, and PRR expression suggested subtle differences in their mechanism of action.

show abstract

Section: Resultsmentioning

confidence: 99%

“…Oxidative stress is a major mechanism which contributes to impaired heart function in diabetes and the RAS has a significant role in the generation of oxidative stress (22, 24, 34). Consistently, a renin inhibitor, which inhibits both intra- and extracellular Ang II formation, completely protected the diabetic heart from oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Direct renin inhibition prevents cardiac dysfunction in a diabetic mouse model: comparison with an angiotensin receptor antagonist and angiotensin-converting enzyme inhibitor

et al. 2013

View full text Add to dashboard Cite

show abstract

“…6 However, these enzymatic antioxidants exhibit reduced expression and activity under diabetic conditions 6,15 because of increased oxidative stress triggered by hyperglycemia. 16 Hyperglycemia triggered-oxidative stress occurs through multiple mechanisms, including increased glucose autoxidation, increased metabolism of glucose through alternative metabolic pathways, increased formation of advanced glycation endproducts, and local activation of renin-angiotensin-aldosterone system. 6 Bioactive chemical compounds that possess antioxidant activities coupled with ability to suppress maladaptive signaling might be of therapeutic benefit in oxidative stress-induced cardiac hypertrophy.…”

Section: Introductionmentioning

confidence: 99%

Naringin Mitigates Cardiac Hypertrophy by Reducing Oxidative Stress and Inactivating c-Jun Nuclear Kinase-1 Protein in Type I Diabetes

Adebiyi

Owira

2016

Journal of Cardiovascular Pharmacology

View full text Add to dashboard Cite

Cardiac hypertrophy (CH) in type 1 diabetes mellitus is attributed to increased oxidative stress-associated activation of c-Jun Nuclear Kinase (JNK). We investigated the effects of naringin on hyperglycemia-associated oxidative stress, activation of JNK-1, and CH. Male Sprague-Dawley rats (225-250 g) (n = 7) were divided into 6 groups. Groups I and II were orally treated with distilled water [3.0 mL/kg body weight/day (BW)] and naringin (50 mg/kg BW), respectively. Groups III-VI were rendered diabetic by a single intraperitoneal injection of 65 mg/kg BW of streptozotocin. Groups III, IV, and V were further treated with insulin (4.0 I.U, s.c, twice daily), naringin (50 mg/kg BW), and ramipril (3.0 mg/kg BW), respectively. After 56 days, the animals were sacrificed and then plasma and cardiac tissues obtained for further analysis. Naringin treatment of diabetic rats significantly reversed oxidative stress, lipid peroxidation, proteins oxidation, CH indices, and JNK protein activation compared with untreated diabetic animals. Our results do suggest that naringin mitigates CH by inhibiting oxidative stress leading to inactivation of JNK-1. Naringin supplements could therefore ameliorate CH in diabetic patients.

show abstract

“…Myocardial ischemia/reperfusion (MI/R) injury occurs inevitably in a wide range of patients, such as survivors of cardiac arrest, victims of acute myocardial infarction, as well as in patients undergoing cardiac surgery (1). MI/R leads to oxidative stress, which subsequently leads to reactive oxygen species (ROS) production, an increase in malondialdehyde (MDA) levels and subsequent cytotoxic injury (2,3).…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effects of exenatide against oxidative stress-induced injury

Chang

Zhang

et al. 2013

International Journal of Molecular Medicine

View full text Add to dashboard Cite

Myocardial ischemia/reperfusion (MI/R) leads to oxidative stress, which may in turn lead to myocardial injury. In the present study, we investigated the effects of exenatide, a glucagon-like peptide-1 (GLP-1) analogue, on oxidative stress-induced injury in vitro and in vivo. In in vitro experiments, H9c2 cells were incubated with exenatide to determine the direct cytoprotective effects of exenatide following exposure to hydrogen peroxide (H2O2). Pre-treatment with exenatide (1 nM), prior to H2O2 exposure, increased cell viability and inhibited H2O2-induced reactive oxygen species (ROS) production. Exenatide also decreased the levels of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) in the cultured supernatants, as well as those of malondialdehyde (MDA) in the H9c2 cells and increased the total superoxide dismutase (T-SOD) levels in the H9c2 cells. In in vivo experiments, an animal model of MI/R was induced by coronary occlusion. Pre-treatment with exenatide (10 µg/kg/day) protected the rat hearts from MI/R-induced injury by decreasing the levels of LDH and CK-MB in plasma, increasing the levels of catalase, T-SOD and glutathione peroxidase (GSH-Px) in the heart and decreasing the MDA levels in the rats with MI/R-induced injury. Exenatide also reduced the infarct size and enhanced cardiac function in the rats with MI/R-induced injury. Moreover, pre-treatment with exenatide inhibited cardiomyocyte apoptosis, increased Aktserine473 and Badserine136 phosphorylation and decreased cleaved caspase-3 expression in vitro and in vivo; however, these effects were attenuated by the phosphoinositide 3-kinase (PI3K) inhibitor, LY294002. Our results suggest that exenatide exerts significant cardioprotective effects against oxidative stress-induced injury in vitro and in vivo. The mechanisms involved may be attributed to the scavenging of oxidative stress products, such as ROS, the increase in the concentrations of antioxidant defense enzymes and the inhibition of cardiomyocyte apoptosis. The anti-apoptotic effects of exenatide were, at least in part, associated with the activation of the PI3K/Akt signaling pathway.

show abstract

Diabetic cardiomyopathy

Cited by 30 publications

References 45 publications

Direct renin inhibition prevents cardiac dysfunction in a diabetic mouse model: comparison with an angiotensin receptor antagonist and angiotensin-converting enzyme inhibitor

Direct renin inhibition prevents cardiac dysfunction in a diabetic mouse model: comparison with an angiotensin receptor antagonist and angiotensin-converting enzyme inhibitor

Naringin Mitigates Cardiac Hypertrophy by Reducing Oxidative Stress and Inactivating c-Jun Nuclear Kinase-1 Protein in Type I Diabetes

Cardioprotective effects of exenatide against oxidative stress-induced injury

Contact Info

Product

Resources

About