title: Exercise mediated protection of diabetic heart through modulation of microRNA mediated molecular pathways.
abstract: Hyperglycaemia, hypertension, dyslipidemia and insulin resistance collectively impact on the myocardium of people with diabetes, triggering molecular, structural and myocardial abnormalities. These have been suggested to aggravate oxidative stress, systemic inflammation, myocardial lipotoxicity and impaired myocardial substrate utilization. As a consequence, this leads to the development of a spectrum of cardiovascular diseases, which may include but not limited to coronary endothelial dysfunction, and left ventricular remodelling and dysfunction. Diabetic heart disease (DHD) is the term used to describe the presence of heart disease specifically in diabetic patients. Despite significant advances in medical research and long clinical history of anti-diabetic medications, the risk of heart failure in people with diabetes never declines. Interestingly, sustainable and long-term exercise regimen has emerged as an effective synergistic therapy to combat the cardiovascular complications in people with diabetes, although the precise molecular mechanism(s) underlying this protection remain unclear. This review provides an overview of the underlying mechanisms of hyperglycaemia- and insulin resistance-mediated DHD with a detailed discussion on the role of different intensities of exercise in mitigating these molecular alterations in diabetic heart. In particular, we provide the possible role of exercise on microRNAs, the key molecular regulators of several pathophysiological processes.
authors.affiliation: Department of Physiology, HeartOtago, University of Otago, 270, Great King Street, Dunedin, 9010, New Zealand.
authors.forename: Jason Kar Sheng
authors.initials: JK
authors.lastname: Lew
authors.affiliation: Department of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.|Biomedicine Discovery Institute and Department of Physiology, Monash University, Clayton, Australia.
authors.forename: James T
authors.initials: JT
authors.lastname: Pearson
authors.affiliation: Department of Physiology, HeartOtago, University of Otago, 270, Great King Street, Dunedin, 9010, New Zealand. daryl.schwenke@otago.ac.nz.
authors.forename: Daryl O
authors.initials: DO
authors.lastname: Schwenke
authors.affiliation: Department of Physiology, HeartOtago, University of Otago, 270, Great King Street, Dunedin, 9010, New Zealand. rajesh.katare@otago.ac.nz.
authors.forename: Rajesh
authors.identifier: 0000-0001-5419-7935
authors.initials: R
authors.lastname: Katare
mesh_terms: D001786:Blood Glucose / Q000502:physiology; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D058065:Diabetic Cardiomyopathies / Q000097:blood* / Q000503:physiopathology / Q000517:prevention & control*; D015444:Exercise / Q000502:physiology*; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D007333:Insulin Resistance / Q000502:physiology; D035683:MicroRNAs / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D035683:MicroRNAs
keywords: Cardioprotection; Cross-talk effect; Diabetic heart disease; Exercise; Hyperglycaemia; Insulin resistance; MicroRNA