ReviewPflugers Archiv : European journal of physiology2004
Channel-induced apoptosis of infected host cells-the case of malaria.
Review in Pflugers Archiv : European journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 94 citations in OpenAlex.
- Phospholipid scramblase 1: a frontline defense against viral infections.Frontiers in cellular and infection microbiology · 2025Review
- Anti-phosphatidylserine antibody levels are low in multigravid pregnant women in a malaria-endemic area in Nigeria, and do not correlate with anti-VAR2CSA antibodies.Frontiers in cellular and infection microbiology · 2023Article
- Pathogen induced subversion of NADCell death discovery · 2021Article
- Insights into the Cytoadherence Phenomenon ofFrontiers in immunology · 2017Review
- Evidencing the Role of Erythrocytic Apoptosis in Malarial Anemia.Frontiers in cellular and infection microbiology · 2016Review
- Triggers, inhibitors, mechanisms, and significance of eryptosis: the suicidal erythrocyte death.BioMed research international · 2015Review
- Breakdown of phosphatidylserine asymmetry following treatment of erythrocytes with lumefantrine.Toxins · 2014Article
- Turning up the heat: heat stress induces markers of programmed cell death in Plasmodium falciparum in vitro.Cell death & disease · 2013Article
- A Type VI secretion system encoding locus is required for Bordetella bronchiseptica immunomodulation and persistence in vivo.PloS one · 2012Article
- Anti-malarial effect of gum arabic.Malaria journal · 2011Article
- Circulating red cell-derived microparticles in human malaria.The Journal of infectious diseases · 2011Article
- Article
- Apoptosis of non-parasitized red blood cells in malaria: a putative mechanism involved in the pathogenesis of anaemia.Malaria journal · 2010Article
- A cell-based high-throughput screen validates the plasmodial surface anion channel as an antimalarial target.Molecular pharmacology · 2010Article
- Malaria parasite mutants with altered erythrocyte permeability: a new drug resistance mechanism and important molecular tool.Future microbiology · 2010Review
- Altered membrane structure and surface potential in homozygous hemoglobin C erythrocytes.PloS one · 2009Article
- Azathioprine favourably influences the course of malaria.Malaria journal · 2009Article
- Potential roles of electrogenic ion transport and plasma membrane depolarization in apoptosis.The Journal of membrane biology · 2006Review
- Ion channels in cell proliferation and apoptotic cell death.The Journal of membrane biology · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of erythrocytes by the malaria pathogen Plasmodium falciparum leads to activation of several distinct anion channels and a non-selective, Ca2+-permeable cation channel. All channel types are presumably activated by the oxidative stress generated by the pathogen. Similar or identical channels are activated by oxidation of non-infected erythrocytes. Activation of the non-selective cation channel allows entry of Ca2+ and Na+, both of which are required for intracellular growth of the pathogen. The entry of Ca2+ stimulates an intraerythrocytic scramblase that facilitates bi-directional phospholipid migration across the bilayer, resulting in breakdown of the phosphatidylserine asymmetry of the cell membrane. The exposure of phosphatidylserine at the outer surface of the cell membrane is presumably followed by binding to phosphatidylserine receptors on macrophages and subsequent phagocytosis of the affected erythrocyte. The lysosomal degradation may eventually eliminate the pathogen. The channel may thus play a dual role in pathogen survival. Absence of the channels is not compatible with pathogen growth, enhanced channel activity accelerates erythrocyte "apoptosis" that may represent a host defence mechanism serving to eliminate infected erythrocytes.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.