ArticlePLoS pathogens2015
Leishmania infantum modulates host macrophage mitochondrial metabolism by hijacking the SIRT1-AMPK axis.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 111 citations in OpenAlex.
- Metabolic sensor AMPK licenses intestinal CD103Science advances · 2026Article
- Article
- Evaluation of Antileishmanial and Antibacterial Activity of Bioconjugate Guanidine-Temporin.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Targeting mitochondrial bioenergetics: the "Achilles' heel" of Leishmania.Parasites & vectors · 2026Article
- Natural product-based therapeutic strategies againstFrontiers in microbiology · 2026Review
- Characterization of the dual functions of Leishmania CK1.2 in both the parasite and the macrophage.PloS one · 2026Article
- Review
- Persistent myeloid cell reprogramming despite miltefosine treatment in leishmania-infected macaques.iScience · 2025Article
- Epigenetic landscape of Leishmania-host interactions.Epigenomics · 2025Review
- The Capsular Polysaccharides GXM and GXMGal fromMicroorganisms · 2025Article
- ENO1 fromBiomolecules · 2025Article
- Lack of Hypoxia Inducible Factor-1α Influences on Macrophages Ability to Deal withJID innovations : skin science from molecules to population health · 2025Article
- Article
- Pharmacological inhibition of key metabolic pathways attenuates Leishmania spp infection in macrophages.PLoS neglected tropical diseases · 2025Article
- The effect of treatment with a non-ionic surfactant vesicular formulation of sodium stibogluconate on host immune responses and serum metabolites in a murine model ofFrontiers in immunology · 2025Article
- Pathogenicity and virulence of African trypanosomes: From laboratory models to clinically relevant hosts.Virulence · 2023Review
- Development of New Leishmanicidal Compounds via Bioconjugation of Antimicrobial Peptides and Antileishmanial Guanidines.ACS omega · 2023Article
- Article
- Roles of ADP-Ribosylation during Infection Establishment byPathogens (Basel, Switzerland) · 2023Review
- BOTH THE INFECTION STATUS AND INFLAMMATORY MICROENVIRONMENT INDUCE TRANSCRIPTIONAL REMODELING IN MACROPHAGES IN MURINE LEISHMANIAL LESIONS.The Journal of parasitology · 2023Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic manipulation of host cells by intracellular pathogens is currently recognized to play an important role in the pathology of infection. Nevertheless, little information is available regarding mitochondrial energy metabolism in Leishmania infected macrophages. Here, we demonstrate that during L. infantum infection, macrophages switch from an early glycolytic metabolism to an oxidative phosphorylation, and this metabolic deviation requires SIRT1 and LKB1/AMPK. SIRT1 or LBK1 deficient macrophages infected with L. infantum failed to activate AMPK and up-regulate its targets such as Slc2a4 and Ppargc1a, which are essential for parasite growth. As a result, impairment of metabolic switch caused by SIRT1 or AMPK deficiency reduces parasite load in vitro and in vivo. Overall, our work demonstrates the importance of SIRT1 and AMPK energetic sensors for parasite intracellular survival and proliferation, highlighting the modulation of these proteins as potential therapeutic targets for the treatment of leishmaniasis.
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.