Cardiomyopathy, the scarring of the heart muscle caused by chronic oxygen deprivation, can be mitigated in part by this inflammatory response, suggests new study.
This reactionary response, according to a new study published in the journal Cell Stem Cell, can counteract part of the scarring—or heart fibrosis—caused by a lack of oxygen.
Professor Richard Harvey of the Victor Chang Cardiac Research Institute in Sydney, Australia, who is the study’s lead author, said the research sheds new light on what happens to the heart’s cells during a heart attack.
“Our gene pathways sense the lack of oxygen, or hypoxia, after a heart attack and mount a protective response.
“If the protective response is blocked, reactive chemicals called oxidants build up in the heart’s cells, including in the beating muscle cells.
“The study has shown that oxidants also build up in the heart’s “fibroblasts”—an important type of heart cell that plays an essential role in healing the heart after a heart attack,” said Professor Harvey.
There is a correlation between oxidant buildup and the expansion of cardiac fibroblasts, which leads to excessive scarring, according to the study. When the heart’s capacity to pump blood properly is hindered by this dense scar tissue, it increases the risk of cardiac failure and sudden cardiac death.
Heart attacks are the biggest cause of death in Australia, with one occurring every 10 minutes. However, there are currently few medications available to successfully prevent or treat the scarring damage that might occur as a result of such an occurrence.
Dr. Vaibhao Janbandhu, a member of the research team from the Victor Chang Cardiac Research Institute, said the findings should spur the development of new treatments.
“Hopefully what we have discovered will lead to the pursuit of synthetic antioxidants that can specifically target different cell types in the heart after a heart attack, including fibroblasts, to limit and even repair some of the damage.”
“This study indicates there is a whole new generation of drugs required—antioxidants—that can be tailored to the responses of particular cells.
“Fibrosis doesn’t just involve the heart but is also seen in other injuries and diseases, so hopefully this work can eventually translate to help other conditions as well,” said Dr. Janbandhu.
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