Why the study?
Does aging induce cardiac diastolic dysfunction, oxidative stress, and accumulation of advanced glycation endproducts in mouse ventricular myocytes?
Population
Ventricular myocytes from young (2-month) and aged (24-26-month) mice
Comparison
Aging (24-26 months) vs Young mice (2 months)
Design
Preclinical
Authors
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Aging impairs myocyte relaxation and stress tolerance in mice; leaves open whether AGEs drive human diastolic dysfunction.
Does aging induce cardiac diastolic dysfunction, oxidative stress, and accumulation of advanced glycation endproducts in mouse ventricular myocytes?
Aging induces cardiac diastolic dysfunction and reduced stress tolerance in mouse cardiomyocytes, which is associated with enhanced oxidative damage and accumulation of advanced glycation endproducts.
Li et al. (2005) studied this question.
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