Right ventricular dysfunction in preclinical models of type I and type II diabetes.

Diabetic cardiomyopathy (DCM) is a growing clinical entity and major health burden characterized by comorbid diabetes mellitus and heart failure. DCM has been commonly associated with impaired function of the left ventricle (LV); however, DCM likely also occurs in the right ventricle (RV) which has distinct physiology and pathophysiology from the LV. RV dysfunction is the strongest determinant of mortality in several clinical contexts yet remains poorly studied in diabetes.

Juvenile physical activity protects against isoproterenol-induced cardiac dysfunction later in life.

Cardiovascular disease is an enormous public health problem, particularly in older populations. Exercise is the most potent cardioprotective intervention identified to date, with exercise in the juvenile period potentially imparting greater protection, given the plasticity of the developing heart. To test the hypothesis that voluntary wheel running early in life would be cardioprotective later in life when risk for disease is high, we provided male and female juvenile (3 wk old) mice access to a running wheel for 2 wk.

Metformin protects against pulmonary hypertension-induced right ventricular dysfunction in an age- and sex-specific manner independent of cardiac AMPK.

Right ventricular (RV) function is the strongest predictor of survival in age-related heart failure as well as other clinical contexts in which aging populations suffer significant morbidity and mortality. However, despite the significance of maintaining RV function with age and disease, mechanisms of RV failure remain poorly understood and no RV-directed therapies exist. The antidiabetic drug and AMP-activated protein kinase (AMPK) activator metformin protects against left ventricular dysfunction, suggesting cardioprotective properties may translate to the RV.

Voluntary Wheel Running Exercise Does Not Attenuate Circadian and Cardiac Dysfunction Caused by Conditional Deletion of .

Circadian misalignment occurs with age, jet lag, and shift work, leading to maladaptive health outcomes including cardiovascular diseases. Despite the strong link between circadian disruption and heart disease, the cardiac circadian clock is poorly understood, prohibiting identification of therapies to restore the broken clock. Exercise is the most cardioprotective intervention identified to date and has been suggested to reset the circadian clock in other peripheral tissues.

Mechanisms of Exercise-Induced Cardiac Remodeling Differ Between Young and Aged Hearts.

Aging induces physiological and molecular changes in the heart that increase the risk for heart disease. Several of these changes are targetable by exercise. We hypothesize that the mechanisms by which exercise improves cardiac function in the aged heart differ from those in the young exercised heart.