heart attack Archives - Sanford Burnham Prebys
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NIH grant aims to boost heart muscle

AuthorMonica May
Date

August 23, 2019

Heart disease is the number one killer of Americans. Now, the National Institutes of Health (NIH) has awarded a four-year grant totaling nearly half a million dollars to Sanford Burnham Prebys to find medicines that could help people repair damaged heart muscle—and potentially reduce the risk of heart attack or other cardiovascular events. 

“Each year we lose far too many loved ones to heart attacks and other heart conditions,” says grant recipient Chris Larson, PhD, adjunct associate professor in the Development, Aging and Regeneration Program at Sanford Burnham Prebys. “Now, we have the opportunity to find medicines that may help more people live long, active lives by strengthening their heart muscles.”

Nearly half of American adults—approximately 120 million people—have cardiovascular disease, according to the American Heart Association and NIH. The condition occurs when blood vessels that supply the heart with oxygen and nutrients become narrowed or blocked, increasing risk of a heart attack, chest pain (angina) or stroke. Current medications for cardiovascular disease can lower blood pressure or thin the blood to minimize risk. Still, five years after a heart attack, 47% of women and 36% of men will die, develop heart failure or experience a stroke. No medicines that repair heart muscle exist. 

To identify drugs that may stimulate heart muscle growth, Larson and his team will screen hundreds of thousands of compounds against human heart muscle cells, called cardiomyocytes. The work will be done in collaboration with Alexandre Colas, PhD, assistant professor in the Development, Aging and Regeneration Program at Sanford Burnham Prebys, who developed the high-throughput screening system that will be employed.

Once the scientists identify drug candidates that promote heart muscle growth, they will study these compounds in additional cellular and animal models of heart disease in the hopes of uncovering insights into the biology behind the repair process. 

“After experiencing a heart attack or other cardiovascular event, many people live in fear that it will happen again,” says Colas. “Today we embark on a journey toward a future where people living with cardiovascular disease don’t have to be afraid of a second heart attack.”

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Scientific breakthrough may limit damage caused by heart attacks

AuthorJessica Moore
Date

June 30, 2016

A research advance from the Sanford Burnham Prebys Medical Discovery Institute (SBP) and Stanford University could lead to new drugs that minimize the damage caused by heart attacks. The discovery, published in Nature Communications, reveals a key control point in the formation of new blood vessels in the heart, and offers a novel approach to treat heart disease patients.

“We found that a protein called RBPJ serves as the master controller of genes that regulate blood vessel growth in the adult heart,” said Mark Mercola, PhD, professor in SBP’s Development, Aging, and Regeneration Program and jointly appointed as professor of medicine at Stanford University, senior author of the study. “RBPJ acts as a brake on the formation of new blood vessels. Our findings suggest that drugs designed to block RBPJ may promote new blood supplies and improve heart attack outcomes.”

In the US, someone has a heart attack every 34 seconds. The ensuing loss of heart muscle, if it affects a large enough area, can severely reduce the heart’s pumping capacity, which causes labored breathing and makes day-to-day tasks difficult. This condition, called heart failure, arises within five years in at least one in four heart attack patients.

The reason heart muscle dies in a heart attack is that it becomes starved of oxygen—a heart attack is caused by blockage of an artery supplying the heart. If heart muscle had an alternative blood supply, more muscle would remain intact, and heart function would be preserved. Many researchers have therefore been searching for ways to promote the formation of additional blood vessels in the heart.

“Studies in animals have shown that having more blood vessels in the heart reduces the damage caused by ischemic injuries, but clinical trials of previous therapies haven’t succeeded,” said Ramon Díaz-Trelles, PhD, staff scientist at SBP and lead author of the study. “The likely reason they have failed is that these studies have evaluated single growth factors, but in fact building blood vessels requires the coordinated activity of numerous factors. Our data show that RBPJ controls the production of these factors in response to the demand for oxygen.

“We used mice that lack RBPJ to show that it plays a novel role in myocardial blood vessel formation (angiogenesis)—it acts as a master controller, repressing the genes needed to create new vessels,” added Diaz-Trelles. “What’s remarkable is that removing RBPJ in the heart muscle did not cause adverse effects—the heart remained structurally and functionally normal in mice without it, even into old age.”

“RBPJ is a promising therapeutic target. It’s druggable, and our findings suggest that blocking it could benefit patients with cardiovascular disease at risk of a heart attack. It may also be relevant to other diseases,” commented Pilar Ruiz-Lozano, PhD, associate professor of pediatrics at Stanford and adjunct professor at SBP, co-senior author. “Inhibitors of RBPJ might also be used to treat peripheral artery disease, and activators might be beneficial in cancer by inhibiting tumor angiogenesis.”

The paper is available online here.

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Hearts build new muscle with this simple protein patch

Authorsgammon
Date

September 15, 2015

An international team of researchers has identified a protein that helps heart muscle cells regenerate after a heart attack. Researchers also showed that a patch loaded with the protein and placed inside the heart improved cardiac function and survival rates after a heart attack in mice and pigs. Continue reading “Hearts build new muscle with this simple protein patch”