[tt] advanced nanotechnology - Calorie restriction anti-aging may operate via mitochondria
Eugen Leitl
<eugen at leitl.org> on
Sun Sep 23 10:21:54 UTC 2007
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To: eugen <eugen at leitl.org>
Subject: advanced nanotechnology - Calorie restriction anti-aging may operate via mitochondria
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"[2]advanced nanotechnology" - 1 new article
1. [3]Calorie restriction anti-aging may operate via mitochondria
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[6]Calorie restriction anti-aging may operate via mitochondria
[7]
Mitochondria play an unexpectedly important role in cell survival in
the face of stress, according to a paper in this week's Cell. The
authors suggest that this cell stress response may provide clues about
how calorie restriction extends lifespan in mammals. This research
also confirms one of the seven parts of the [8]SENS strategy for life
extension.
[9]del.icio.us
[10]Sinclair, working with colleagues at his company, at Cornell
University in New York and the U.S. National Institutes of Health,
identified the actions of two more sirtuin genes called SIRT3 and
SIRT4. They found the enzymes controlled by these genes help preserve
the mitochondria -- little organs inside of cells that provide their
energy.
Researchers report in the journal Cell that the phenomenon is
likely linked to two enzymes--SIRT3 and SIRT4--in mitochondria (the
cell's powerhouse that, among other tasks, converts nutrients to
energy). They found that a cascade of reactions triggered by lower
caloric intake raises the levels of these enzymes, leading to an
increase in the strength and efficiency of the cellular batteries.
By invigorating the mitochondria, SIRT3 and SIRT4 extend the life
of cells, by preventing flagging mitochondria from developing tiny
holes (or pores) in their membranes that allow proteins that
trigger apoptosis, or cell death, to seep out into the rest of the
cell.
"We didn't expect that the most important part of this pathway was
in the mitochondria," says David Sinclair, an assistant professor
of pathology at Harvard Medical School and a study co-author. "We
think that we've possibly found regulators of aging."
"As long as the mitochondria are physiologically active, the cell
can otherwise be depleted of energy, but it stays alive," Sinclair
said.
"I think SIRT3 is the next most interesting sirtuin from a drug
development standpoint," Sinclair says. "It does protect cells, but
there's growing evidence that it may mediate the benefits of
exercise as well."
Sinclair's lab is now working on developing what he calls a
possible "supermouse" with elevated levels of NAMPT to see if it
lives longer and is more disease-resistant than normal mice.
Sinclair is eager to see the results of his experiments with the
supermouse. "Depending on how this mouse turns out," he says, "we
may put NAMPT on the list of drug targets, as well."
[11]The recent SENS3 (on using engineering approaches to life
extension) conference discussed several methods to repair and preserve
mitochondria Mitochondrial damage is one of seven kinds of damage
resulting from aging which if the damage was prevented or greatly
reduced or repaired could result in lifespans increasing by several
decades. This study also provides more evidence that the SENS approach
is likely to succeed because one of the seven causes of damage
identified by SENS has been separately confirmed as having an
antiaging effect when modified.
[12]Sirtris Pharmaceuticals shares rose 11% after release of the study
results
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blood product transfusion [del.icio.us]
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8. http://www.sens.org/
9. http://del.icio.us/post?url=http://advancednano.blogspot.com/2007/09/calorie-restriction-anti-aging-may.html&title=Calorie%20restrictions%20anti%20aging%20effects%20operates%20via%20healthier%20mitochondria.%20Mitochondria%20repair%20is%20one%20of%20the%20seven%20mechanism%20of%20the%20SENS%20engineering%20strategy%20to%20life%20extension
10. http://www.sciam.com/article.cfm?articleID=242CBE56-E7F2-99DF-37DEAE209E877BFB&chanID=sa007
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Eugen* Leitl <a href="http://leitl.org">leitl</a> http://leitl.org
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