Aging as a substrate of heart failure.
Heart failure is a typical age-associated disease. However, the mechanism by which heart function declines and heart failure increases in association with age is not clear. Recent advances in basic science clarify several important mechanisms of aging. The mechanisms identified are likely to serve as substrates by which heart function declines and predisposes elderly people to heart failure. One such mechanism is insulin/insulin-like growth factor (IGF)-1 signaling. Suppression of insulin/IGF-1 signaling prevents cardiac aging associated with improved protein homeostasis in the heart. However, the role of insulin/IGF-1 signaling in heart diseases is likely to be pleiotropic, and both protective and sensitizing effects have been described in different contexts. Reduction in function of extra-cardiac organs is likely to be another important mechanism by which heart failure increases with aging, since heart failure is a multiple organ system disease.
Department of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan. tshioi@kuhp.kyoto-u.ac.jp
Tetsuo
T
Shioi
Yasutaka
Y
Inuzuka
D000375:Aging / Q000473:pathology / Q000502:physiology*; D000818:Animals; D001343:Autophagy / Q000502:physiology; D004249:DNA Damage; D006333:Heart Failure / Q000209:etiology*; D006706:Homeostasis; D006801:Humans; D007249:Inflammation / Q000209:etiology; D007328:Insulin / Q000502:physiology; D007334:Insulin-Like Growth Factor I / Q000502:physiology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology; D046988:Proteasome Endopeptidase Complex / Q000502:physiology; D011506:Proteins / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D016615:Telomere / Q000502:physiology; D025801:Ubiquitin / Q000502:physiology
D007328:Insulin; D011506:Proteins; D025801:Ubiquitin; D007334:Insulin-Like Growth Factor I; D046988:Proteasome Endopeptidase Complex