After heart attack injury, several fatty-acid-derived bioactive molecules — including one called resolvin D1 — play an essential signaling role to safely clear inflammation and help repair heart muscle. The mechanism of how this resolution occurs is not well-understood.

There is a receptor on the surface of many immune cells called ALX/FRP2, and in models of atherosclerosis, ALX/FPR2 is known to act as a sensor to help resolve inflammation.

In a 2015 study using a mouse model, University of Alabama at Birmingham esearcher Ganesh Halade, Ph.D., observed that, after heart attack injury, ALX/FPR2 was highly expressed in immune myeloid cells and was activated by resolvin D1 in immune cells in the spleen and in immune cells at the heart attack site. The result was an expedited resolution of the heart attack injury. Resolvin D1 is one of the omega 3 fatty-acid metabolites known as specialized pro-resolving mediators, or SPMs, that help clear inflammation.

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