Malaria claims over 600,000 lives each year, and with climate change, the disease’s range is expanding. Although some drugs can prevent and treat malaria, resistance to these medications is increasing.
Researchers at the University of Utah Health have identified a new target for antimalarial drugs: a protein called DMT1. This protein helps malaria parasites access iron, which is crucial for their survival and reproduction. Their findings suggest that drugs blocking DMT1 could be highly effective against malaria.
The Importance of Iron
Paul Sigala, PhD, an associate professor at the Spencer Fox Eccles School of Medicine, explains that iron is vital for the survival of malaria parasites. Without it, they die quickly. However, acquiring iron from human red blood cells, where the parasites live, is complex. The parasites must extract iron-rich hemoglobin from the blood, break it down, and transport the iron to essential parts of their cells.
Uncovering a Key Player
Researchers suspected DMT1 was essential for the parasites’ iron usage because it resembles genes involved in metal transport in other organisms. They found that DMT1 is critical for parasite survival. By editing the parasites’ genome, they could turn off DMT1 production. When DMT1 was disabled, the parasites died quickly, unable to infect more blood cells.
This rapid death highlights the importance of iron transport in many processes within the parasites. Sigala notes, “Blocking this protein impairs nearly all aspects of parasite viability during blood-stage infection.”
Promising Results
The research confirmed that DMT1 is crucial for iron transport. When the researchers reduced DMT1 activity, the parasites survived but grew more slowly. Interestingly, providing extra iron helped restore their growth. The remaining DMT1 proteins could transport enough iron to support normal growth when iron was abundant. However, without DMT1, no amount of iron could save the parasites.
A New Drug Target
The researchers are optimistic that DMT1 could be a viable target for new antimalarial drugs. Kade Loveridge, a graduate researcher, explains that DMT1 is similar enough to human iron transporters for identification but different enough to allow for the creation of a parasite-specific inhibitor with minimal effects on humans.
The quick death of parasites when DMT1 is turned off is encouraging. If a drug can be developed to inhibit DMT1, it may act faster than current treatments. The team is now testing existing iron transport inhibitors to see if they can serve as antimalarial drugs.
Loveridge adds that their discovery may pave the way for future research into the parasite’s growth and potential treatments. “We’re cracking the door,” he says. “I hope others can throw it wide open.”
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