ArticleCell death & disease2013
Malaria parasite liver stages render host hepatocytes susceptible to mitochondria-initiated apoptosis.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed.
- Systems analysis of immune responses to attenuated P. falciparum malaria sporozoite vaccination reveals excessive inflammatory signatures correlating with impaired immunity.PLoS pathogens · 2022Trial
- Evolution of Resistance to Avian Malaria Infection in an Endemic Hawaiian Honeycreeper.Ecology and evolution · 2026Article
- Host kinase regulation of Plasmodium vivax dormant and replicating liver stages.PLoS neglected tropical diseases · 2026Article
- Comparative immunological study of Plasmodium knowlesi infections in humans and macaques: insights into cytokine dynamics.Malaria journal · 2025Article
- Long lived liver-resident memory T cells of biased specificities for abundant sporozoite antigens drive malaria protection by radiation-attenuated sporozoite vaccination.PLoS pathogens · 2025Article
- Pathogen-induced mitochondrial dysfunction: mechanistic insights, immune crosstalk, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Antiplasmodial evidence, host mitochondrial biology and possible mechanisms of action of a composite extract ofJournal of parasitic diseases : official organ of the Indian Society for Parasitology · 2024Article
- Hepatocytes and the art of killing Plasmodium softly.Trends in parasitology · 2024Review
- Correlative light-electron microscopy methods to characterize the ultrastructural features of the replicative and dormant liver stages of Plasmodium parasites.Malaria journal · 2024Article
- Association of apoptosis-related variants to malaria infection and parasite density in individuals from the Brazilian Amazon.Malaria journal · 2023Article
- Plasmodium's fight for survival: escaping elimination while acquiring nutrients.Trends in parasitology · 2022Review
- Red Blood Cell BCL-xMicroorganisms · 2022Article
- Hexane fraction ofToxicology reports · 2022Article
- Liver-stage fate determination inFrontiers in microbiology · 2022Article
- Recent Advances in Host-Directed Therapies for Tuberculosis and Malaria.Frontiers in cellular and infection microbiology · 2022Review
- Host-parasite interactions duringFrontiers in immunology · 2022Review
- Mitochondria as a Cellular Hub in Infection and Inflammation.International journal of molecular sciences · 2021Review
- Host-directed therapy, an untapped opportunity for antimalarial intervention.Cell reports. Medicine · 2021Review
- Review
- Elucidating Spatially-Resolved Changes in Host Signaling DuringFrontiers in cellular and infection microbiology · 2021Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Intracellular eukaryotic parasites and their host cells constitute complex, coevolved cellular interaction systems that frequently cause disease. Among them, Plasmodium parasites cause a significant health burden in humans, killing up to one million people annually. To succeed in the mammalian host after transmission by mosquitoes, Plasmodium parasites must complete intracellular replication within hepatocytes and then release new infectious forms into the blood. Using Plasmodium yoelii rodent malaria parasites, we show that some liver stage (LS)-infected hepatocytes undergo apoptosis without external triggers, but the majority of infected cells do not, and can also resist Fas-mediated apoptosis. In contrast, apoptosis is dramatically increased in hepatocytes infected with attenuated parasites. Furthermore, we find that blocking total or mitochondria-initiated host cell apoptosis increases LS parasite burden in mice, suggesting that an anti-apoptotic host environment fosters parasite survival. Strikingly, although LS infection confers strong resistance to extrinsic host hepatocyte apoptosis, infected hepatocytes lose their ability to resist apoptosis when anti-apoptotic mitochondrial proteins are inhibited. This is demonstrated by our finding that B-cell lymphoma 2 family inhibitors preferentially induce apoptosis in LS-infected hepatocytes and significantly reduce LS parasite burden in mice. Thus, targeting critical points of susceptibility in the LS-infected host cell might provide new avenues for malaria prophylaxis.
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