Diabetische Kardiomyopathie

Stratmann, Bernd; Stork, I.; Tschöepe, Diethelm

doi:10.1007/s00108-008-2047-6

Cited by 6 publications

(3 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Metabolic impairment such as hyperglycemia, hyperlipidemia, hypoinsulinemia, and alterations in cardiac metabolism are the main reasons for vascular structural and functional changes, which instigate the cellular effects leading to redox imbalance, interstitial fibrosis, myocyte death, and disturbances in ion transport and homeostasis [43]. A decrease in myosin ATPase, a shift in myosin isoenzyme distribution, alterations in a variety of Ca 2+ fluxes associated with cardiac mechanical alterations are observed in experimental DM [44].…”

Section: Experimental Diabetes-induced Cardiovascular Complicationsmentioning

confidence: 99%

Glycoxidative Stress and Cardiovascular Complications in Experimentally-Induced Diabetes: Effects of Antioxidant Treatment

Karasu¹

2010

TOCMJ

View full text Add to dashboard Cite

Diabetes mellitus (DM) is a common metabolic disease, representing a serious risk factor for the development of cardiovascular complications, such as coronary heart disease, peripheral arterial disease and hypertension. Oxidative stress (OS), a feature of DM, is defined as an increase in the steady-state levels of reactive oxygen species (ROS) and may occur as a result of increased free radical generation and/or decreased anti-oxidant defense mechanisms. Increasing evidence indicates that hyperglycemia is the initiating cause of the tissue damage in DM, either through repeated acute changes in cellular glucose metabolism, or through long-term accumulation of glycated biomolecules and advanced glycation end products (AGEs). AGEs are formed by the Maillard process, a non-enzymatic reaction between ketone group of the glucose molecule or aldehydes and the amino groups of proteins that contributes to the aging of proteins and to the pathological complications of DM. In the presence of uncontrolled hyperglycemia, the increased formation of AGEs and lipid peroxidation products exacerbate intracellular OS and results in a loss of molecular integrity, disruption in cellular signaling and homeostasis, followed by inflammation and tissue injury such as endothelium dysfunction, arterial stiffening and microvascular complications. In addition to increased AGE production, there is also evidence of multiple pathways elevating ROS generation in DM, including; enhanced glucose auto-oxidation, increased mitochondrial superoxide production, protein kinase C-dependent activation of NADPH oxidase, uncoupled endothelial nitric oxide synthase (eNOS) activity, increased substrate flux through the polyol pathway and stimulation of eicosanoid metabolism. It is, therefore, not surprising that the correction of these variables can result in amelioration of diabetic cardiovascular abnormalities. A linking element between these phenomena is cellular redox imbalance due to glycoxidative stress (GOS). Thus, recent interest has focused on strategies to prevent, reverse or retard GOS in order to modify the natural history of diabetic cardiovascular abnormalities. This review will discuss the links between GOS and diabetes-induced cardiovascular disorders and the effect of antioxidant therapy on altering the development of cardiovascular complications in diabetic animal models.

show abstract

Section: Experimental Diabetes-induced Cardiovascular Complicationsmentioning

confidence: 99%

Glycoxidative Stress and Cardiovascular Complications in Experimentally-Induced Diabetes: Effects of Antioxidant Treatment

Karasu¹

2010

TOCMJ

View full text Add to dashboard Cite

show abstract

“…Under diabetic conditions, myocardial cells are exposed to multiple pathological stimuli, such as hyperglycemia, dyslipidemia, hyperinsulinemia, and oxidative stress [2]. All of which injure cardiac cells, either directly or indirectly, resulting in abnormalities in structure and function, including cardiac apoptosis, interstitial fibrosis, myocardial hypertrophy, and heart failure [3]. …”

Section: Introductionmentioning

confidence: 99%

Resveratrol Modulates Apoptosis and Autophagy Induced by High Glucose and Palmitate in Cardiac Cells

Liu

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Diabetic cardiomyopathy is associated with increased apoptosis and suppressed autophagy in cardiac cells. The polyphenol resveratrol has shown beneficial effects in various cardiovascular diseases. This study investigated if resveratrol protected cardiac cells by modulating apoptosis and autophagy in the context of diabetes. Methods: H9c2 cardiac myoblast cells were exposed to high glucose combined with palmitate. Autophagy was evaluated by estimating LC3-II/I ratio, P62 protein levels, and LC3 fluorescent puncta. Apoptosis was assessed by using terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL), flow cytometry, and analysis of the protein expression of apoptotic markers (cleavage of caspase-3 and PARP). Results: High glucose and palmitate suppressed autophagic activity and exacerbated apoptotic cell death in cardiac myoblast cells. Resveratrol restored autophagy and attenuated apoptosis in cells upon diabetic stimuli. Moreover, resveratrol activated AMPK and JNK1, thereby suppressing mTOR and its downstream effectors p70S6K1 and 4EBP1, as well as disrupting the Beclin1–Bcl-2 complex. Conclusion: Resveratrol protects cardiac cells by regulating the switch between autophagy and apoptotic machinery under diabetic conditions, which is attributed by AMPK-mediated phosphorylation of mTORC1/p70S6K1/4EBP1 and JNK-mediated dissociation of Beclin1-Bcl-2. Our study suggests that autophagy may be an important target for resveratrol in the treatment of diabetic cardiomyopathy.

show abstract

“…It was postulated that these modifications are consequences of the altered cardiac metabolism found in type 2 diabetes and are relevant for the stability of the myocardial cytoskeleton. The impact of type 2 diabetes on cardiomyopathy, termed “diabetic cardiomyopathy,” is under debate (18). …”

mentioning

confidence: 99%