title: Views from within and beyond: narratives of cardiac contractile dysfunction under senescence.
abstract: Senescence is associated with enhanced risk of cardio-vascular diseases. It is generally considered that decline in growth hormones (such as insulin-like growth factor I), intrinsic myocardial and endothelial functions, as well as accumulation of reactive oxygen species with increased age may contribute to cardiovascular senescence. It is believed that heart function, especially cardiac reserve declines with advanced age. However, most experimental and clinical investigations on ventricular function only included young or adult subjects and failed to address this important age issue in heart pathophysiology. Although senescent but otherwise healthy hearts may possess normal pumping function at the resting or non-stressed state, some aging-associated factors such as accumulation of reactive oxygen species and activation of selective stress signaling path-ways may interact with certain risk factors and compromise overall cardiac function. The precise cause and progression of compromised cardiac function in the elderly remain controversial. This review will focus on senescence-related alterations in cardiac contractile function with a special emphasis on oxidative stress and activation of stress signaling.
authors.affiliation: Division of Pharmaceutical Sciences and Center for Cardiovascular Research and Alternative Medicine, University of Wyoming, Laramie, WY 82071, USA.
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Yang
authors.forename: Nair
authors.initials: N
authors.lastname: Sreejayan
authors.forename: Jun
authors.initials: J
authors.lastname: Ren
mesh_terms: D000368:Aged; D000375:Aging / Q000502:physiology*; D000818:Animals; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology*; D004703:Endocrine System / Q000503:physiopathology; D005260:Female; D006321:Heart / Q000502:physiology*; D006801:Humans; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D032383:Myocytes, Cardiac / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D015398:Signal Transduction / Q000502:physiology