Diabetic cardiomyopathy: a hyperglycaemia- and insulin-resistance-induced heart disease

Diabetic cardiomyopathy is characterised in its early stages by diastolic relaxation abnormalities and later by clinical heart failure in the absence of dyslipidaemia, hypertension and coronary artery disease. Insulin resistance, hyperinsulinaemia and hyperglycaemia are each independent risk factors...

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Veröffentlicht in:Diabetologia Jg. 61; H. 1; S. 21 - 28
Hauptverfasser: Jia, Guanghong, Whaley-Connell, Adam, Sowers, James R.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Berlin/Heidelberg Springer Berlin Heidelberg 01.01.2018
Springer Nature B.V
Schlagworte:
Aldosterone
Angiotensin
Animals
Cardiomyopathy
Cardiovascular disease
Coronary artery
Coronary artery disease
Diabetes
Diabetes mellitus
Diabetic Cardiomyopathies - blood
Diabetic Cardiomyopathies - physiopathology
Disease resistance
Dyslipidemia
Endothelial cells
Exosomes
Fibrosis
Heart diseases
Heart Diseases - blood
Heart Diseases - physiopathology
Heart failure
Human Physiology
Humans
Hyperglycemia
Hyperglycemia - blood
Hyperglycemia - physiopathology
Immunomodulation
Insulin
Insulin resistance
Insulin Resistance - physiology
Internal Medicine
Medicine
Medicine & Public Health
Metabolic Diseases
Metabolic rate
Oxidative stress
Renin
Review
Risk factors
Heart failure
Insulin resistance
Hyperglycaemia
Review
Cardiac dysfunction
ISSN:0012-186X, 1432-0428, 1432-0428
Online-Zugang:Volltext
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Zusammenfassung:Diabetic cardiomyopathy is characterised in its early stages by diastolic relaxation abnormalities and later by clinical heart failure in the absence of dyslipidaemia, hypertension and coronary artery disease. Insulin resistance, hyperinsulinaemia and hyperglycaemia are each independent risk factors for the development of diabetic cardiomyopathy. The pathophysiological factors in diabetes that drive the development of cardiomyopathy include systemic metabolic disorders, inappropriate activation of the renin–angiotensin–aldosterone system, subcellular component abnormalities, oxidative stress, inflammation and dysfunctional immune modulation. These abnormalities collectively promote cardiac tissue interstitial fibrosis, cardiac stiffness/diastolic dysfunction and, later, systolic dysfunction, precipitating the syndrome of clinical heart failure. Recent evidence has revealed that dysregulation of coronary endothelial cells and exosomes also contributes to the pathology behind diabetic cardiomyopathy. Herein, we review the relationships among insulin resistance/hyperinsulinaemia, hyperglycaemia and the development of cardiac dysfunction. We summarise the current understanding of the pathophysiological mechanisms in diabetic cardiomyopathy and explore potential preventative and therapeutic strategies.
Bibliographie:ObjectType-Article-1
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ObjectType-Feature-2
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ObjectType-Literature Review-3
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ISSN:0012-186X
1432-0428
1432-0428
DOI:10.1007/s00125-017-4390-4