ArticleCell reports2020
Mycobacterium tuberculosis Limits Host Glycolysis and IL-1β by Restriction of PFK-M via MicroRNA-21.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
What it found
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Who cites it
112 citing papers in PubMed, 160 citations in OpenAlex.
- Monocyte metabolic transcriptional programs associate with resistance to tuberculin skin test/interferon-γ release assay conversion.The Journal of clinical investigation · 2021Trial
- MicroRNA-1246 regulates macrophage lipid metabolism and is involved in resistance to human Mycobacterium tuberculosis infection.PLoS pathogens · 2026Article
- Regulation of Inducible Nitric Oxide Synthase (NOS2) Expression in Healthy and Inflamed Bowel: A Narrative Review.International journal of molecular sciences · 2026Review
- Article
- Mycobacterium tuberculosis MEM39 (Rv1977) hijacks host aldolase A (ALDOA) to subvert immunometabolism to facilitate bacterial intracellular survival.Cellular & molecular immunology · 2026Article
- Inflammasome activation dictates the efficacy of antimycobacterial activity of frontline TB drugs.PLoS pathogens · 2026Article
- HSV-1-Driven Lipid Metabolic Reprogramming and Lipid Droplet Accumulation in Macrophages Impair Antiviral Immunity.Investigative ophthalmology & visual science · 2026Article
- Myeloid-derived alveolar-like macrophages are a tractable model to understand the role of ontogeny in alveolar macrophage functionbioRxiv : the preprint server for biology · 2026Article
- HIV inhibits Warburg metabolism in human macrophages infected with Mycobacterium tuberculosis.Scientific reports · 2026Article
- Non-coding RNAs in lipid metabolism and their roles in atherosclerosis.Nature reviews. Cardiology · 2026Review
- The immunometabolic topography of cellular organization and bacterial control in tuberculosis granulomas.Nature immunology · 2026Article
- IFN-γ-induced trained immunity enhances killing of priority pathogens in healthy and genetically vulnerable individuals.JCI insight · 2026Article
- MicroRNAs as Orchestrators of Immune Responses to Bacterial Infection.Microorganisms · 2026Review
- Integrating single-cell RNA-seq and bulk RNA-seq to identify hub pathways and diagnostic biomarkers in active pulmonary tuberculosis.BMC infectious diseases · 2026Article
- A Key Metabolic Protein in Active Mycobacterium tuberculosis: Insights into Carbon, Nitrogen, and Sulfur Metabolism.Advances in experimental medicine and biology · 2026Review
- Molecular signaling in coinfection: howFrontiers in immunology · 2026Review
- Metabolic reprogramming of macrophages during mycobacterial infection: a review of immunometabolic crosstalk and pathogen manipulation.Frontiers in cellular and infection microbiology · 2026Review
- Host miRNA orchestration of mitophagy pathways during bacterial infection: current advances and future directions.Frontiers in microbiology · 2026Review
- Metabolic reprogramming of immune cells in the battle against intracellular bacterial chronic infections: novel mechanisms and breakthroughs.Molecular biology reports · 2025Review
- Machine learning identifies MiRNA biomarkers and immune mechanisms in active tuberculosis.Scientific reports · 2025Article
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Increased glycolytic metabolism recently emerged as an essential process driving host defense against Mycobacterium tuberculosis (Mtb), but little is known about how this process is regulated during infection. Here, we observe repression of host glycolysis in Mtb-infected macrophages, which is dependent on sustained upregulation of anti-inflammatory microRNA-21 (miR-21) by proliferating mycobacteria. The dampening of glycolysis by miR-21 is mediated through targeting of phosphofructokinase muscle (PFK-M) isoform at the committed step of glycolysis, which facilitates bacterial growth by limiting pro-inflammatory mediators, chiefly interleukin-1β (IL-1β). Unlike other glycolytic genes, PFK-M expression and activity is repressed during Mtb infection through miR-21-mediated regulation, while other less-active isoenzymes dominate. Notably, interferon-γ (IFN-γ), which drives Mtb host defense, inhibits miR-21 expression, forcing an isoenzyme switch in the PFK complex, augmenting PFK-M expression and macrophage glycolysis. These findings place the targeting of PFK-M by miR-21 as a key node controlling macrophage immunometabolic function.
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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.