Contribution of impaired insulin signaling to the pathogenesis of diabetic cardiomyopathy
Zamora, Mònica (Institut d'Investigacions Biomèdiques August Pi i Sunyer)
Villena, Josep A. (Hospital Universitari Vall d'Hebron)
Universitat Autònoma de Barcelona

Data:	2019
Resum:	Diabetic cardiomyopathy (DCM) has emerged as a relevant cause of heart failure among the diabetic population. Defined as a cardiac dysfunction that develops in diabetic patients independently of other major cardiovascular risks factors, such as high blood pressure and coronary artery disease, the underlying cause of DCMremains to be unveiled. Several pathogenic factors, including glucose and lipid toxicity, mitochondrial dysfunction, increased oxidative stress, sustained activation of the renin-angiotensin system (RAS) or altered calcium homeostasis, have been shown to contribute to the structural and functional alterations that characterize diabetic hearts. However, all these pathogenic mechanisms appear to stem from the metabolic inflexibility imposed by insulin resistance or lack of insulin signaling. This results in absolute reliance on fatty acids for the synthesis of ATP and impairment of glucose oxidation. Glucose is then rerouted to other metabolic pathways, with harmful effects on cardiomyocyte function. Here, we discuss the role that impaired cardiac insulin signaling in diabetic or insulin-resistant individuals plays in the onset and progression of DCM.
Ajuts:	Ministerio de Economía y Competitividad BFU2015-64462R
Drets:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Llengua:	Anglès
Document:	Article ; recerca ; Versió publicada
Matèria:	Insulin resistance ; Diabetes ; Heart ; Diabetic cardiomyopathy ; Metabolic flexibility
Publicat a:	International journal of molecular sciences, Vol. 20 Núm. 11 (june 2019) , p. 2833, ISSN 1422-0067

DOI: 10.3390/ijms20112833
PMID: 31212580

16 p, 1.3 MB

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