CELL SIGHTING: Investigators identify senescent cells—those that have lost the ability to divide—by their color. They turn blue when exposed to a particular chemical.
In Brief
- Senescent cells—which have permanently lost the ability to divide—were once assumed to contribute to aging by undermining tissue repair. Cells were thought to enter senescence to avoid becoming cancerous when damage put them at risk of proliferating uncontrollably.
- Later, the notion that senescent cells play a part in the aging of tissues and bodies fell out of favor. More recently, though, that idea has gained new support.
- Recent research indicates that the cells can contribute to aging in the originally proposed way and also by spurring inflammation. Plus, they can harm nearby cells in ways that promote cancer.
- Some evidence in mice suggests that retarding cellular senescence may help slow aging and delay some of the ills associated with it.
More In This Article
In 1999 Jan M. Van Deursen and his colleagues at the Mayo Clinic in Rochester, Minn., wanted to see whether mangled chromosomes cause cancer. So they engineered mice deficient in a protein that helps to maintain chromosomal integrity. The rodents' coils of DNA were duly deranged. Surprisingly, though, the animals were not particularly tumor-prone. Instead they developed a strange grab bag of ills, including cataracts, dwindling muscles, rapid thinning of fat under the skin and progressive spinal curvature, that made them look like one-humped camels. They also tended to die young.
Van Deursen had no idea why those particular abnormalities showed up. Then, in 2002, he spotted a report on mice afflicted by accelerated aging and was struck by photographs showing that their backs became humped as they aged. Suddenly, it hit him: his camel-backed mice, too, were aging unusually fast. Probing deeper, the Mayo team discovered that cells in a number of the rodents' tissues had prematurely slid into a state called cellular senescence, in which cells permanently lose the ability to divide and become aberrant in other ways. Such failure of cell division would explain the bone, muscle, eye and skin abnormalities observed by van Deursen's group.
This article was originally published with the title Quiet Little Traitors.
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3 Comments
Add CommentI've often wondered if aging is a form of cancer that can be cured or sent into remission like any other form of cancer.
Reply | Report Abuse | Link to thisEating a proper diet, which means one which contains all of the amino acids necessary for human protein generation, the essential omega oils, all of the minerals, all of the A and B vitamins, and Vitamin E, and one is exposed to sun light, sufficient to generate Vitamin D, and, finally if one is active, one can avoid most 'diseases,' including cancer, and have a good and healthy outlook on life. Of course you will need good genes to take advantage of this lifestyle. And, as healthy as you may be, you still have a meeting with the grim reaper. It seems that our cells cannot divide forever, and when cells begin to fail so also does our plumbing, our electrical system, and even our skeleton. Senescence is a nice word for failure due to aging.
Reply | Report Abuse | Link to thisAlthough the article seems to paint the picture that cellular senescence has more cons than pros, the law of evolution dictates that the two should be in balance. If, for example, senescent cells are doing more harm than good, then evolution should have eliminated them long ago. Conversely, if they are doing more good than harm, then cells should turn senescent earlier than they do now. It is thus no surprise that killing senescent cells in rodents do not prolong their lives.
Reply | Report Abuse | Link to thisOf course humans may be exception to the above argument because our lifestyles have been changing faster than evolution can catch up, but if that is the case, it doesn't make sense to draw any conclusions from rodent experiments.