"We show that macrophages -- white blood cells primarily known for removing cellular debris, pathogens and other unwanted materials -- are actively involved in the development of HFpEF," says Maarten Hulsmans, PhD, a research fellow in the MGH Center for Systems Biology and lead author of the paper. "These findings put macrophages on the map when it comes to HFpEF therapy and open up previously unexplored treatment options."
The concept of heart failure traditionally referred to a loss of the organ's pumping capacity, which is called systolic heart failure. But in HFpEF the heart retains the ability to pump or eject blood into the circulation. What is compromised is the ability of the heart muscle to relax and allow blood to flow into the left ventricle, reducing the amount of blood available to pump into the aorta. Symptoms of HFpEF are similar to those of heart failure in general, but since factors contributing to the condition are not well understood, it has been difficult to find promising therapies.
Interactions - Cells - Heart - Macrophages - Function
Interactions among cells within the heart -- including macrophages -- are essential to normal cardiac function but can also contribute to problems. For example, after the heart muscle is damaged by a heart attack, macrophages induce the cells called fibroblasts to generate the connective tissues that help reinforce damaged tissue. But excessive fibroblast activation can lead to the distortion and stiffening of tissues, further reducing cardiac function.
To explore a potential role for macrophages in HFpEF, the MGH team examined cardiac macrophages in two mouse models that develop the...
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