Israeli scientists, discovering that increasing the supply of a certain protein in mice led to raising their life expectancy by 23% and reducing their susceptibility to cancer, are speculating that the same effect may be found on humans.
The scientists note in the abstract to their peer-reviewed research, “Aging leads to a gradual decline in physical activity and disrupted energy homeostasis. The NAD+-dependent SIRT6 deacylase regulates aging and metabolism through mechanisms that largely remain unknown. Here, we show that SIRT6 overexpression leads to a reduction in frailty and lifespan extension in both male and female B6 mice. … These findings show that SIRT6 optimizes energy homeostasis in old age to delay frailty and preserve healthy aging.”
One of the authors of the study, which was published in Nature Communications, Prof. Haim Cohen of Bar-Ilan University, theorized, “The change in life expectancy is significant, when you consider that an equivalent jump in human life expectancy would have us living on average until almost 120. The changes we saw in mice may be translatable to humans, and if so that would be exciting.”
“Cohen’s lab is working on identifying drugs that may allow the SIRT6 protein to safely be boosted in humans,” The Times of Israel reports, adding, “In 2012 Cohen became the first researcher to to actually increase levels in animals and increase life expectancy, and in doing so cause male mice to live 15% longer. But that experiment had no impact on female mice.”
The latest research includes both male and female mice; the mice displayed less cholesterol, less cancer, and more speed.
“This discovery shows that SIRT6 controls the rate of healthy aging, and this shows that boosting its activity could potentially slow aging. … We are developing small molecules that may increase the levels SIRT6, or make existing amounts of the protein more active. They may be used in the future to address aging,” Cohen said.
A study published in “Frontiers in Cell Development and Biology” stated, “Deficiency of SIRT6 induces chronic inflammation, autophagy disorder and telomere instability. Also, these cellular processes can lead to the occurrence and progression of cardiovascular diseases (CVDs), such as atherosclerosis, hypertrophic cardiomyopathy and heart failure.” It added, “In the cardiovascular system, SIRT6 plays a protective function by improving vascular endothelial dysfunction to some extent, delaying the formation of atherosclerotic plaques and inhibiting cardiac hypertrophy and heart failure. In addition, several studies showed that SIRT6 is a principal regulator of glucose metabolism homeostasis.”
Another study pointed out, “DNA double-strand breaks (DSB) are the most deleterious type of DNA damage. In this work, we show that SIRT6 directly recognizes DNA damage through a tunnel-like structure that has high affinity for DSB. SIRT6 relocates to sites of damage independently of signaling and known sensors. … Our findings indicate that SIRT6 plays a previously uncharacterized role as a DNA damage sensor, a critical factor in initiating the DNA damage response.”
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Source: Dailywire
