Many of us remember our parents coaxing us to eat our vegetables, particularly the ones loaded with iron. It’s supposed to make us strong, just like the cartoon “Popeye” and his spinach. Well, iron-containing molecules play a wide range of important roles in the body, including transporting oxygen in the bloodstream.
However, a study done with mice suggests that in case of heart failure, the release of stored iron in the heart may contribute to the death of heart muscle cells. The study focuses on the concern that prolonged use of iron supplements may contribute to higher risk of heart failure.
In a person with heart failure, the heart muscles weaken and become less effective in pumping blood around the body. Symptoms include feeling tired most of the time, breathlessness after exercise or even at rest, and swelling of the ankles and legs. Unfortunately, heart failure is incurable and usually worsens over time, however, with the proper treatment, the symptoms can be controlled for many years.
About 5.7 million people in the US have this condition, according to the National Heart, Lung, and Blood Institute. Heart failure is known to disturb iron metabolism, causing iron deficiency in about 50% of those afflicted with the condition. However, it is unclear whether these changes in the processing of iron are harmful, or actually protect the heart from further damage.
Having said that, a new study by researchers at King’s College London, and Osaka Medical College and Osaka University, in Japan, suggests that excess levels of free iron in the heart could worsen heart failure. The research, which was done with mice, discovered that when iron was released from stores in heart cells, it creates highly reactive, oxygen-containing free radicals (known at times as reactive oxygen species) that damage the heart muscle.
According to Dr. Jumpei Ito, first study author, “Iron is essential for many processes in the body including oxygen transport, but too much iron can lead to a buildup of unstable oxygen molecules that can kill cells.” Dr. Ito was a research associate in the Department of Cardiovascular Sciences at King’s College London (KCL), and is now a visiting scientist at Osaka Medical College.
The new study has safety concerns about prolonged iron supplementation. Particularly on clinical trials that have shown that giving intravenous iron to people with iron deficiency and heart failure improves their symptoms.
Senior author Professor Kinya Otsu, a British Heart Foundation Professor of Cardiology at KCL, had this to say: “Patients with heart failure who are iron deficient are currently treated with iron supplements, which previous studies have shown reduces their symptoms. While our work does not contradict those studies, it does suggest that reducing iron-dependent cell death in the heart could be a potential new treatment strategy for patients.”
To uncover the effect of free iron on heart cells during heart failure, the research team investigated what would happen, if contrary to the usual course of events, the iron remained locked up in a protein called ferritin that stores it. When levels of free iron are low another protein called NCOA4 triggers the release of the stored iron from the ferritin in cells.
The researchers created mice that lack the gene for creating NCOA4 in their heart muscle cells. When heart failure was simulated in these mice, as well as normal mice, they found the hearts of the genetically altered mice sustained fewer harmful changes. Specifically, the mice deficient in NCOA4 did not develop excessive levels of free iron or the toxic free radicals that kill cells during heart failure.
Dr. Ito concluded, “Our results suggest that the release of iron can be detrimental to the heart.” He further added, “It can lead to unstable oxygen levels, death in heart cells, and ultimately heart failure.”
Therefore, drugs that inhibit the release of stored iron from heart cells may be part of a promising new treatment. There is a compound called ferrostatin-1 that inhibits the release of stored iron. When normal mice were treated with ferrostatin-1, it protected their hearts against the cell death that occurs in heart failure.
But note that these are preliminary findings using mice. It would take more studies to understand the process of iron release, and whether inhibiting the release would benefit people with heart failure. But, there is always hope, and with the way scientific research is going, it won’t take long to come out with new medical miracles.
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