Childhood Chemotherapy can Alter Heart’s Caretaker Cells

Children undergoing chemotherapy with anthracyclines may experience heart damage later in life as anthracyclines alter the function of cardiac fibroblasts, the hearts caretaker cells.

Chemotherapy for cancer changes the functions of the cells that repair heart injury, according to a new study by researchers at the University of Texas Health Science Center at San Antonio ( UT Health San Antonio).

The study published in //PLOS ONE found that 20% of the children treated with anthracyclines go on to suffer heart failure later in life.

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‘Chemotherapy with anthracyclines can alter the function of cardiac fibroblasts, the hearts caretaker cells. Childhood chemotherapy could damage heart cells and lead to heart failure.’
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Cardiac fibroblast is a type of caretaker cell in the heart and other tissues of the body.

The researchers believe that damage to the cardiac fibroblast cells may play a role when childhood cancer survivors become adults.

The researchers are studying the effect of a tumor-suppressor gene called p53 has an impact on the response of cardiac fibroblasts to anthracyclines. The tumor suppressor gene p53 generally protects genes from damage.

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The researchers found that when mouse cells without p53 were exposed to anthracyclines, the function of fibroblast was altered. Normal fibroblasts can migrate to help repair the injury in the heart. However, cardiac fibroblasts, when treated with anthracycline, showed lesser migration.

The researchers have not established whether or no less migration is detrimental.

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Currently, pediatric oncologists provide lower doses of anthracycline chemotherapy as compared to when the drugs were introduced four decades ago. Thus, cases of heart failure brought on acutely by the chemotherapy are now rare.

The researchers suggest that heart cells may still be damaged even though there isn’t heart failure or decline in heart function.

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Though there are other types of cells in the heart, the researchers focus on cardiac fibroblasts.

"The overarching hypothesis we have in the lab is that damage to this cell population, the cardiac fibroblast, isn't innocuous," Dr. Aune said. "These cells can have their properties changed by exposure to gene-damaging agents. And then theoretically over time, that may be one contributor to the late effects that we see."

"That might translate into an inability to respond to insults such as high blood pressure or heart attacks because fibroblasts are so important in dealing with an injury," Dr. Mancilla said.

Source-Medindia