Plasmodium falciparum lipid metabolism

Plasmodium falciparum lipid metabolism encompasses the integrated biochemical pathways—including synthesis, scavenging, and modification—that the malaria parasite uses to meet its intense lipid requirements during its life cycle (Nwobodo et al., 2011). During the intra-erythrocytic stage, the parasite undergoes massive membrane biogenesis to support the formation of daughter merozoites, relying on both a prokaryotic-like Type II fatty acid synthesis (FASII) pathway in its apicoplast and the de novo CDP-choline (Kennedy) pathway for phospholipid production (Waller et al., 2003; Mitamura & Palacpac, 2003). Because these pathways contain enzymes and transporters that are either absent or significantly different in the human host, they represent promising targets for antimalarial intervention (Vial et al., 2003). Drugs such as triclosan and thiolactomycin target the FASII pathway components, while albitiazolium disrupts phosphatidylcholine synthesis by blocking choline entry, ultimately leading to parasite death through impaired membrane integrity and organelle development (Ancelin & Vial, 1986; Vial et al., 2003).

Other names

Plasmodium lipid biosynthetic pathwaysMalarial lipid metabolismP. falciparum lipid metabolic pathways

Inhibition of the Type II fatty acid synthesis (FASII) pathway in the apicoplast, disruption of the de novo cytidine diphosphate (CDP)-choline pathway for phosphatidylcholine synthesis, and blockade of choline transport across the parasite membrane.