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Heart Repairs Itself After Heart Attack June 9, 2011

Posted by Metabiological in Longevity.
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Anyone who has or knows someone who has gone through a heart attack knows what a painful and traumatic event it is.  As the number one killer in the US and high up there among other developed countries finding a cure for heart disease would go a long ways towards combating premature death.  Well, some researchers at University College may be on the way to doing just that.

Heart muscle cells, or cardiomyocytes, are irreparably damaged by heart attack. For the heart to continue functioning properly, the damaged cells must be replaced. Heart progenitor cells — cells that can form the various tissues that make up the heart, such as blood vessels and muscle — do exist, but in adults are not active enough to repair damage. So Paul Riley at University College London Institute of Child Health and his colleagues have found a way to wake them up.

The researchers examined the hearts of mice at various time points after the operation. They found heart cells expressing Wt1 just two days after the injury. The cells were initially in the heart’s outer layer, but by two weeks after surgery they had moved inside and clustered around the site of the injury. The cells had also changed in size and shape, and looked just like cardiomyocytes.

Awesome.  Now if they can just figure out how to make the human body turn the switch on and off so to speak.

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Mammalian Hearts Capable of Regrowing February 26, 2011

Posted by Metabiological in Longevity, Transhumanism.
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One of the primary reasons that heart disease is the number one killer in the developed world is the fact that once heart muscle is damaged it is incapable of regrowing.  Or so we thought.

The researchers found that within three weeks of removing 15 percent of the newborn mouse heart, the heart was able to completely grow back the lost tissue, and as a result looked and functioned just like a normal heart. The researchers believe that uninjured beating heart cells, called cardiomyocytes, are a major source of the new cells. They stop beating long enough to divide and provide the heart with fresh cardiomyocytes.

I’m somewhat surprised that rather than cardiac stem cells playing a role in the process the new cells seem to grow from existing mature heart tissue.  Considering the researchers mentioned the heart cells needing to stop beating in order for the division to take place it makes me wonder if that may have something to do with this feature being lost as we grow older.  For an adult individual needing to largely fend for itself the loss of some cardiac output could represent a severe loss in fitness, a difference that may not be overcome by the benefit of being able to regenerate damaged heart cells.

Now of course all the usual caveats apply.  This was in mice not humans.  Its only one study.  It only works in juvenile hearts.  But as a proof on concept it is very exciting especially given the aforementioned seriousness of heart disease as both an individual and societal problem for much of the west.

Gene In Kidney May Predispose You To Heart Disease January 23, 2011

Posted by Metabiological in Longevity, Transhumanism.
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Next up in our series “Nature is COMPLICATED” (there is no series, I just made that up) a study out of the NIH has for the first time found a gene variant in the population that actually seems to cause heart disease.  The kicker?  The gene in question is not even expressed in your heart.

The unexpected results highlight the advantage of performing genome-wide studies to find DNA sequence variants associated with disease.

“I was surprised by the finding,” says Thomas P. Cappola, MD, assistant professor of medicine at the University of Pennsylvania School of Medicine, also a lead investigator on the study. “This is a good example of how taking unbiased approaches to study human disease can lead you to unexpected targets.”

Studying three groups of Caucasian patients with heart failure, they found one DNA sequence variant that was common in all the groups and was actively involved in making an important protein for the body. A single change in the DNA sequence of a gene called CLCNKA leads to a change from arginine to glycine in the 83rd amino acid of the protein. This protein makes up part of a kidney channel responsible for controlling the secretion of chloride ions into the urine, an important process in maintaining the proper balance of salt and water in the body.

That single amino acid change reduced the channel’s ability to shuttle chloride ions across the cell membrane by about half. Dorn hypothesizes that a result of this reduction could be elevated levels of a hormone called renin in the blood. Renin is produced in the kidney and is the first signal in a cascade that can damage the heart. This opens the possibility of helping people who have the variant reduce their risk of heart failure with drugs commonly used to treat high blood pressure, including ACE-inhibitors and aldosterone blockers.

Interesting for a few reasons.  One is obvious, this study has the potential to lead to novel treatments for reducing the risk of heart disease, which as the number one killer in America is something we desperately need to do.  It’s simple utilitarian calculation; reducing risk will not only reduce or eliminate the suffering on those who would other wise have contracted heart disease but will also work to reduce health care costs and ease the burden said costs are placing on society at large.

Second, and more relevant to this blog, it showcases one of the difficulties we face in attempting to increase human longevity.  Namely, nature is COMPLICATED and our bodies are no exception.  As Neil Shubin put it the human body is essentially a retrofitted fish and regardless of how far we’ve come in our evolutionary history we are still bound by that ancestral framework.  As such, attempting to artificially lengthen the human lifespan by figuring out which gene does what and tweaking it appropriately is going to be absurdly difficult.  What once coded for scales may now code for skin and a single gene may do multiple things depending on when and how it is expressed.

This is why Aubrey deGrey’s SENS approach makes a lot of sense, cleaning up the damage of aging rather than attempting to fix the underlying causes.  Whether it ends up working or not is of course another story since no matter what we do we can’t escape the fact that biological life is messy.