ArticleNature communications2015
Dietary restriction protects against experimental cerebral malaria via leptin modulation and T-cell mTORC1 suppression.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05457881 (Short-Term Endogenous Hydrogen Sulfide Upregulation For Vein Graft Disease), which is not on this map. Cited by 48 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Short-Term Endogenous Hydrogen Sulfide Upregulation For Vein Graft Disease
Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Rapamycin not dietary restriction improves resilience against pathogens: a meta-analysis.GeroScience · 2023Pooled it
- Dietary restriction in aging and longevity.Nature aging · 2026Review
- Interplay of obesity and parasitic infection: current evidence of immunogenesis, tumorigenesis and leptin receptor involvement.Nutrition & metabolism · 2025Review
- NR2F6 as a Disease Driver and Candidate Therapeutic Target in Experimental Cerebral Malaria.Cells · 2025Article
- β-hydroxybutyrate inhibits Plasmodium falciparum development and confers protection against malaria in mice.Nature metabolism · 2025Article
- From fat storage to immune hubs: the emerging role of adipocytes in coordinating the immune response to infection.The FEBS journal · 2025Review
- Immune regulation of host energy metabolism and periodicity of malaria parasites.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Mouse NOD/Shi and NSY/Hos strains infected with Plasmodium berghei ANKA are models for experimental cerebral malaria.Experimental animals · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Hormones in malaria infection: influence on disease severity, host physiology, and therapeutic opportunities.Bioscience reports · 2024Review
- Pathogenetic mechanisms and treatment targets in cerebral malaria.Nature reviews. Neurology · 2023Review
- Beyond energy balance regulation: The underestimated role of adipose tissues in host defense against pathogens.Frontiers in immunology · 2023Review
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- An update on cerebral malaria for therapeutic intervention.Molecular biology reports · 2022Review
- Hypothyroidism confers tolerance to cerebral malaria.Science advances · 2022Article
- Thymus, undernutrition, and infection: Approaching cellular and molecular interactions.Frontiers in nutrition · 2022Review
- Mannose inhibitsFrontiers in immunology · 2022Article
- Cerebral malaria induced byFrontiers in cellular and infection microbiology · 2022Review
- Pediatric Cerebral Malaria.Current tropical medicine reports · 2021Article
- Fever: Could A Cardinal Sign of COVID-19 Infection Reduce Mortality?The American journal of the medical sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Host nutrition can affect the outcome of parasitic diseases through metabolic effects on host immunity and/or the parasite. Here we show that modulation of mouse immunometabolism through brief restriction of food intake (dietary restriction, DR) prevents neuropathology in experimental cerebral malaria (ECM). While no effects are detected on parasite growth, DR reduces parasite accumulation in peripheral tissues including the brain, and increases clearance in the spleen. Leptin, a host-derived adipokine linking appetite, energy balance and immune function, is required for ECM pathology and its levels are reduced upon DR. Recombinant leptin abrogates DR benefits, while pharmacological or genetic inhibition of leptin signalling protects against ECM. DR reduces mTORC1 activity in T cells, and this effect is abrogated upon leptin administration. Furthermore, mTORC1 inhibition with rapamycin prevents ECM pathology. Our results suggest that leptin and mTORC1 provide a novel mechanistic link between nutrition, immunometabolism and ECM pathology, with potential therapeutic implications for cerebral malaria.
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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.