a new study out of the University of South Florida into the sirtuins, and in particular Sirt1 and Sirt3, has retuned some very promising results for those who suffer from an acute heart attack.
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https://onlinelibrary.wiley.com/doi/10.1111/acel.13419
https://www.sciencedaily.com/releases/2021/08/210824104133.htm
https://bit.ly/3sIrPjv
https://haleplushearty.org/2021/08/24/age-related-decline-in-two-sirtuin-enzymes-alters-mitochondrial-dynamics-weakens-cardiac-contractions/
https://tgihealthcareerp.com/health-news/age-related-decline-in-two-sirtuin-enzymes-alters-mitochondrial-dynamics-weakens-cardiac-contractions/
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Sirtuins are a family of anti-aging proteins that help regulate cellular lifespan, metabolism, and resistance to stress. The potential protective effect of sirtuins in age-related diseases, including cardiovascular diseases, remains an area of intense investigation, with many Labs worldwide spending enormous amounts of time and money on ground-breaking research. In a new preclinical study led by the University of South Florida Health, researchers have determined that sirtuin 1 (SIRT1) and sirtuin 3 (SIRT3) levels decline in aging hearts; disrupting the ability of cardiac muscle cells to contract in response to reperfusion injury. Furthermore, age-related SIRT1 and SIRT3 deficiency can impair cardiac function by altering mitochondrial dynamics; the researchers report that ‘the mitochondria play a vital role in metabolic health and inflammatory response.’
Our mitochondria produce the energy needed to drive nearly all the processes in our living cells. Cardiac muscle cells contain more mitochondria than any other cells in the body, this because the heart needs large amounts of energy to constantly pump blood throughout the body. Stabile mitochondrial dynamics maintain a healthy balance between the constant division (called fission) and the merging (called fusion) of mitochondria – and helps ensure the quality of these specialized structures more commonly known as the “powerhouse” of the cell.
Reperfusion therapy is a common treatment that includes drugs and surgery. It is performed following an acute heart attack; it restores blood flow (and therefore oxygen) to the region of the heart damaged by the heart attack. Unfortunately, in some patients this necessary procedure triggers further injury to the heart-muscle-tissue surrounding the initial heart attack site. Regrettably, no effective therapies currently exist to prevent reperfusion injury.
To help analyze the response of cardiac mitochondria to reperfusion stress, the researchers deleted SIRT1 or SIRT3 in the cardiac muscle cells of mouse hearts, and then examined the mitochondrial response to stress caused by restricted blood flow. The researchers found that the mitochondria in mouse hearts lacking SIRT3 were more vulnerable to reperfusion stress than the mouse hearts with their SIRT3 intact. The cardiac mitochondrial dynamics (including shape, size, and structure of the mitochondria) in these knockout mice, physiologically resembled that of aged normal mice retaining cardiac SIRT3. Furthermore, the young mice with SIRT1 or SIRT3 removed had measurably weaker cardiomyocyte contractions
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