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Now, a new preclinical study by the University of South Florida Health (Universal Service Fund Health) researchers has determined that sirtuin protein 1 (SIRT1) and sirtuin protein 3 (SIRT3) levels decline, aging the heart, and affect the ability of cardiomyocytes ( Cardiomyocytes) contract against ischemia-reperfusion injury (also called reperfusion injury)
The results of this study were published in the July 3 issue of "Aging Cells"
"We found that age-related changes in mitochondrial dynamics are caused by SIRT1/SIRT3 deficiency, especially in cardiomyocytes," said lead researcher Dr.
In living cells, mitochondria produce the energy needed to drive almost all processes
Reperfusion is a common treatment after an acute heart attack, which restores blood flow (and thus oxygen) in the area of the heart that has been damaged by a clot blocking the coronary arteries
To help analyze the response of myocardial mitochondria to ischemia-reperfusion stress, researchers at USF Health deleted SIRT1 or SIRT3 in mouse cardiomyocytes and tested the response of mitochondria to ischemic stress by restricting blood flow
In addition, when the ischemia-reperfusion stress was introduced, the contraction of the cardiomyocytes of the young mice with SIRT1 or SIRT3 removed was significantly reduced and showed senescence-like cardiac dysfunction
"We started this study to try to understand why the incidence of heart attacks among older people is higher than that of young people, and why even if they receive maximum treatment, they are more likely to die
Dr.
If the results of their mouse model study can be applied to the human heart, Dr.
"Our ultimate goal is to determine the ideal target for the treatment of heart disease, especially for elderly patients," said Dr.
Journal Reference :
Jingwen Zhang, Zhibin He, Julia Fedorova, Cole Logan, Lauryn Bates, Kayla Davitt, Van Le, Jiayuan Murphy, Melissa Li, Mingyi Wang, Edward G.