title: An overview of the inflammatory signalling mechanisms in the myocardium underlying the development of diabetic cardiomyopathy.
abstract: Heart failure is a highly morbid and mortal clinical condition that represents the last stage of most cardiovascular disorders. Diabetes is strongly associated with an increased incidence of heart failure and directly promotes cardiac hypertrophy, fibrosis, and apoptosis. These changes, in turn, contribute to the development of ventricular dysfunction. The clinical condition associated with the spectrum of cardiac abnormalities induced by diabetes is termed diabetic cardiomyopathy. Myocardial inflammation has recently emerged as a pathophysiological process contributing to cardiac hypertrophy, fibrosis, and dysfunction in cardiac diseases. Myocardial inflammation is also implicated in the development of diabetic cardiomyopathy. Several molecular mechanisms link diabetes to myocardial inflammation. The NF-κB signalling pathway and the renin-angiotensin-aldosterone system are strongly activated in the diabetic heart, thereby promoting myocardial inflammation. Advanced glycation end-products and damage-associated molecular pattern molecules also represent strong triggers for inflammation. The mediators resulting from this inflammatory process modulate specific intracellular signalling mechanisms in cardiac cells that promote the development of diabetic cardiomyopathy. This review article will provide an overview of the signalling molecular mechanisms linking diabetic cardiomyopathy to myocardial inflammation.
authors.affiliation: Department of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, 04100 Latina (LT), Italy.|Department of AngioCardioNeurology, IRCCS Neuromed, 86077 Pozzilli (IS), Italy.
authors.forename: Giacomo
authors.initials: G
authors.lastname: Frati
authors.affiliation: Department of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, 04100 Latina (LT), Italy.
authors.forename: Leonardo
authors.initials: L
authors.lastname: Schirone
authors.affiliation: Department of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, 04100 Latina (LT), Italy.
authors.forename: Isotta
authors.initials: I
authors.lastname: Chimenti
authors.affiliation: Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO, 63110, USA.
authors.forename: Derek
authors.initials: D
authors.lastname: Yee
authors.affiliation: Department of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, 04100 Latina (LT), Italy.|Department of AngioCardioNeurology, IRCCS Neuromed, 86077 Pozzilli (IS), Italy.
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Biondi-Zoccai
authors.affiliation: Department of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, 04100 Latina (LT), Italy.|Department of AngioCardioNeurology, IRCCS Neuromed, 86077 Pozzilli (IS), Italy.
authors.forename: Massimo
authors.initials: M
authors.lastname: Volpe
authors.affiliation: Department of Medical and Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, 04100 Latina (LT), Italy.|Department of AngioCardioNeurology, IRCCS Neuromed, 86077 Pozzilli (IS), Italy.
authors.forename: Sebastiano
authors.initials: S
authors.lastname: Sciarretta
mesh_terms: D000818:Animals; D058065:Diabetic Cardiomyopathies / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D005355:Fibrosis; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D011379:Prognosis; D015398:Signal Transduction
chemical_list: D018836:Inflammation Mediators
keywords: Cardiomyopathy; Cytokine; Diabetes; Heart failure; Inflammation