Diabetic cardiomyopathy: an update of mechanisms contributing to this clinical entity
By Guanghong Jia, M. Hill, J. Sowers. Circulation Research, 2018
1,476 citations recorded by the source corpus.
Heart failure and related morbidity and mortality are increasing at an alarming rate, in large part, because of increases in aging, obesity, and diabetes mellitus. The clinical outcomes associated with heart failure are considerably worse for patients with diabetes mellitus than for those without diabetes mellitus. In people with diabetes mellitus, the presence of myocardial dysfunction in the absence of overt clinical coronary artery disease, valvular disease, and other conventional cardiovascular risk factors, such as hypertension and dyslipidemia, has led to the descriptive terminology, diabetic cardiomyopathy. The prevalence of diabetic cardiomyopathy is increasing in parallel with the increase in diabetes mellitus. Diabetic cardiomyopathy is initially characterized by myocardial fibrosis, dysfunctional remodeling, and associated diastolic dysfunction, later by systolic dysfunction, and eventually by clinical heart failure. Impaired cardiac insulin metabolic signaling, mitochondrial dysfunction, increases in oxidative stress, reduced nitric oxide bioavailability, elevations in advanced glycation end products and collagen-based cardiomyocyte and extracellular matrix stiffness, impaired mitochondrial and cardiomyocyte calcium handling, inflammation, renin–angiotensin–aldosterone system activation, cardiac autonomic neuropathy, endoplasmic reticulum stress, microvascular dysfunction, and a myriad of cardiac metabolic abnormalities have all been implicated in the development and progression of diabetic cardiomyopathy. Molecular mechanisms linked to the underlying pathophysiological changes include abnormalities in AMP-activated protein kinase, peroxisome proliferator-activated receptors, O-linked N-acetylglucosamine, protein kinase C, microRNA, and exosome pathways. The aim of this review is to provide a contemporary view of these instigators of diabetic cardiomyopathy, as well as mechanistically based strategies for the prevention and treatment of diabetic cardiomyopathy.
Subfields: Cardiology and Cardiovascular Medicine, Endocrinology, Diabetes and Metabolism, Neurology
View Paper: https://www.semanticscholar.org/paper/59e449a9dabe38322eff7d6ee6ae8cd499504cee
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Endocrinology, Diabetes and Metabolism
- T. Hansen
- J. Beulens
- L. Rydén
- E. Dal Canto
- Antonio Ceriello
- Oliver Schnell
- M. Ferrini
- Eberhard Standl
Citations in the corpus
- Insulin resistance, cardiovascular stiffening and cardiovascular disease. (2021, neutral): “Collectively, over time these vascular hemodynamic disturbances promote left ventricular remodeling and fi brosis and left ventricular diastolic dysfunction (i.e. heart failure with preserved systolic function (HFpSF)) and development of coronary artery disease [25 – 28].”
- Diabetes as a cardiovascular risk factor: An overview of global trends of macro and micro vascular complications (2019, background): “Initial subclinical cardiac abnormalities of DMCMP, such as LV fibrosis and increased LV stiffness, might occur independently of diabetes duration and quality of metabolic control and can progress to symptomatic HF.(9,20) In diabetes clinical trials, subjects with HF are poorly represented and there”