The inflammatory response following a heart attack affects another organ too: the kidneys. From the University of Alabama at Birmingham, scientists investigate a bioactive compound, resolvin D1, and its ability to protect the kidneys from tissue damage following a heart attack.
In the heart, tissue damage from a heart attack stretches the left ventricle and contributes to heart failure. Heart disease and kidney disease are intricately connected, as the heart’s job is to pump blood and the kidneys’ job is to filter the blood, removing waste and extra water. The two conditions are both exacerbated by high blood pressure and diabetes.
A bioactive compound called resolvin D1 has been shown in the past to - as its name suggests - resolve the inflammatory response that naturally occurs as the body’s reaction to heart attack. Inflammation is healthy as an initial, short-lived response to heart attack. Immune cells called macrophages engulf dead and dying cells through a process called phagocytosis. But if inflammation goes on too long, it can do more harm than good in both the heart and the kidneys.
Resolvin D1, naturally produced by the immune system to prevent the inflammatory response from going overboard, can also limit the damage from kidney inflammation after heart attack. The new University of Alabama at Birmingham study highlights four specific ways resolvin D1 does it:
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Induces immune cells to leave the damaged heart tissue to prevent too much inflammation
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Expedites the macrophage transition to their reparative role instead of their phagocytic role
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Regulates microRNA activity, increasing the amount of regenerative micrRNAs, which control gene expression after a heart attack
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Reduces kidney damage by removing white blood cells
Researchers from the study tested resolvin D1 in a mice model of heart attack. Some mice were given therapeutic doses of the bioactive compound and some were not. The mice who were not given resolvin D1 experienced significant variation in microRNA activity and exhibited various signs of kidney inflammation after heart attack. Mice who did receive resolvin D1 had fewer regulatory changes in microRNA and did not show the same signs of kidney damage.
Resolvin D1 has yet to be studied in humans to confirm its ability to reduce kidney damage after a heart attack outside the context of mice. But if human studies were to validate the compound’s effectiveness, it could make a huge difference in a clinical setting for people recovering after a heart attack.
The present study was published in The FASEB Journal.
Sources: American Journal of Pathology, National Kidney Foundation, Journal of Molecular and Cellular Cardiology, University of Alabama at Birmingham
