Microparticle Therapy Reduces Damage Following Heart Attack
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The change we'd like to see in medicine is a move away from fixing things after high-mortality-risk events, and towards preventing those events from occurring in the first place. All too much of modern medical research is focused on rebuilding and patching up survivors, rather than addressing the root causes of fatal age-related conditions. Better rebuilding and patching does provide some improvement in the state of affairs, and when it is all you can do it is a good approach - but this is no longer all that can be done. We live in an age in which the causes of degenerative aging and all age-related disease are known and can be worked on.

If even a tenth of the research effort that goes into fixing heart damage went into preventing heart damage by repairing the cellular and molecular damage that causes aging, we'd all be far better off. That said, this technology looks like it may have far broader applications than just reducing the impact of heart attack damage on survivors:

After a heart attack, much of the damage to the heart muscle is caused by inflammatory cells that rush to the scene of the oxygen-starved tissue. But that inflammatory damage is slashed in half when microparticles are injected into the blood stream within 24 hours of the attack. When biodegradable microparticles were injected after a heart attack, the size of the heart lesion was reduced by 50 percent and the heart could pump significantly more blood.

The particles are made of poly(lactic-co-glycolic) acid [and] are designed to have a negative charge on their surface. This makes them irresistible to the inflammatory monocytes, which have a positively charged receptor. When the inflammatory cell bonds to the microparticle, a signal on the cell is activated that announces it's dying and ready for disposal. The cell then travels to the spleen, the natural path for the removal of dying cells, rather than going to the site of the inflammation.

The scientists' study showed the microparticles reduced damage and repaired tissue in many other inflammatory diseases. These include models of West Nile virus, colitis, inflammatory bowel disease, multiple sclerosis, peritonitis and a model that mimics blood flow after a kidney transplant. "We're very excited. The potential for this simple approach is quite extraordinary. Inflammatory cells pick up immune-modifying microparticles and are diverted down a natural pathway used by the body to dispose of old cells. It's amazing that such a simple detour limits major tissue damage in such a wide range of diseases."

Link: http://www.eurekalert.org/pub_releases/2014-01/nu-had010914.php

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