ArticleBlood2015
Red cells from ferrochelatase-deficient erythropoietic protoporphyria patients are resistant to growth of malarial parasites.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Targeting Infected Host Cell Heme Metabolism to Kill Malaria Parasites.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Towards next-generation treatment options to combat Plasmodium falciparum malaria.Nature reviews. Microbiology · 2025Review
- Review
- Role of Host Small GTPases in Apicomplexan Parasite Infection.Microorganisms · 2022Review
- Small-molecule inhibitors of ferrochelatase are antiangiogenic agents.Cell chemical biology · 2022Article
- Host-parasite interactions duringFrontiers in immunology · 2022Review
- Network-Based Approaches Reveal Potential Therapeutic Targets for Host-Directed Antileishmanial Therapy Driving Drug Repurposing.Microbiology spectrum · 2021Article
- Three Signatures of Adaptive Polymorphism Exemplified by Malaria-Associated Genes.Molecular biology and evolution · 2021Article
- Re-Envisioning Anti-Apicomplexan Parasite Drug Discovery Approaches.Frontiers in cellular and infection microbiology · 2021Review
- Host Porphobilinogen Deaminase Deficiency Confers Malaria Resistance inFrontiers in cellular and infection microbiology · 2020Article
- Manipulation of autophagy for host-directed tuberculosis therapy.African journal of thoracic and critical care medicine · 2019Review
- Host genetics in malaria: lessons from mouse studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Erythrocytes lacking the Langereis blood group protein ABCB6 are resistant to the malaria parasiteCommunications biology · 2018Article
- Plasmodium heme biosynthesis: To be or not to be essential?PLoS pathogens · 2017Review
- Antimalarial drug resistance: linking Plasmodium falciparum parasite biology to the clinic.Nature medicine · 2017Review
- Article
- Griseofulvin impairs intraerythrocytic growth of Plasmodium falciparum through ferrochelatase inhibition but lacks activity in an experimental human infection study.Scientific reports · 2017Article
- The apicoplast: now you see it, now you don't.International journal for parasitology · 2017Review
- Distinct Prominent Roles for Enzymes of Plasmodium berghei Heme Biosynthesis in Sporozoite and Liver Stage Maturation.Infection and immunity · 2016Article
- A case of erythropoietic protoporphyria.Proceedings (Baylor University. Medical Center) · 2016Article
Corrections and comments
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Authors and funding
16 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many red cell polymorphisms are a result of selective pressure by the malarial parasite. Here, we add another red cell disease to the panoply of erythrocytic changes that give rise to resistance to malaria. Erythrocytes from individuals with erythropoietic protoporphyria (EPP) have low levels of the final enzyme in the heme biosynthetic pathway, ferrochelatase. Cells from these patients are resistant to the growth of Plasmodium falciparum malarial parasites. This phenomenon is due to the absence of ferrochelatase and not an accumulation of substrate, as demonstrated by the normal growth of P falciparum parasites in the EPP phenocopy, X-linked dominant protoporphyria, which has elevated substrate, and normal ferrochelatase levels. This observation was replicated in a mouse strain with a hypomorphic mutation in the murine ferrochelatase gene. The parasite enzyme is not essential for parasite growth as Plasmodium berghei parasites carrying a complete deletion of the ferrochelatase gene grow normally in erythrocytes, which confirms previous studies. That ferrochelatase is essential to parasite growth was confirmed by showing that inhibition of ferrochelatase using the specific competitive inhibitor, N-methylprotoporphyrin, produced a potent growth inhibition effect against cultures of P falciparum. This raises the possibility of targeting human ferrochelatase in a host-directed antimalarial strategy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.