ArticleFrontiers in neuroscience2014
Lactate transport and receptor actions in cerebral malaria.
Article in Frontiers in neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Succinate and lactate produced as conserved biomarkers through chronic and transient substrate-level phosphorylation: from microorganisms to cancer.Journal of bioenergetics and biomembranes · 2026Review
- Review
- Article
- Alteration of Blood Lactate Levels in Severe Falciparum Malaria: A Systematic Review and Meta-Analysis.Biology · 2021Review
- Whole blood transfusion improves vascular integrity and increases survival in artemether-treated experimental cerebral malaria.Scientific reports · 2021Article
- The inhibitory effect of LPS on the expression of GPR81 lactate receptor in blood-brain barrier model in vitro.Journal of neuroinflammation · 2018Article
- Lactate Transport and Receptor Actions in Retina: Potential Roles in Retinal Function and Disease.Neurochemical research · 2016Review
- A probable dual mode of action for both L- and D-lactate neuroprotection in cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- Glycolysis at 75: is it time to tweak the first elucidated metabolic pathway in history?Frontiers in neuroscience · 2015Article
- Potential role of Plasmodium falciparum-derived ammonia in the pathogenesis of cerebral malaria.Frontiers in neuroscience · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral malaria (CM), caused by Plasmodium falciparum infection, is a prevalent neurological disorder in the tropics. Most of the patients are children, typically with intractable seizures and high mortality. Current treatment is unsatisfactory. Understanding the pathogenesis of CM is required in order to identify therapeutic targets. Here, we argue that cerebral energy metabolic defects are probable etiological factors in CM pathogenesis, because malaria parasites consume large amounts of glucose metabolized mostly to lactate. Monocarboxylate transporters (MCTs) mediate facilitated transfer, which serves to equalize lactate concentrations across cell membranes in the direction of the concentration gradient. The equalizing action of MCTs is the basis for lactate's role as a volume transmitter of metabolic signals in the brain. Lactate binds to the lactate receptor GPR81, recently discovered on brain cells and cerebral blood vessels, causing inhibition of adenylyl cyclase. High levels of lactate delivered by the parasite at the vascular endothelium may damage the blood-brain barrier, disrupt lactate homeostasis in the brain, and imply MCTs and the lactate receptor as novel therapeutic targets in CM.
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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.