ReviewImmunology2012
Molecular mechanisms of metabolic reprogramming in proliferating cells: implications for T-cell-mediated immunity.
Review in Immunology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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
46 citing papers in PubMed, 84 citations in OpenAlex.
- N-Carbamylglutamate Promotes Growth and Immunity in Danzhou Chickens via Gut Microbiota-Metabolite Interactions Involving Sphingolipid and mTOR Pathways.Microorganisms · 2026Article
- Deciphering the MYCN-driven metabolic microenvironment of neuroblastoma.Trends in molecular medicine · 2026Review
- Integrative multi-omics and machine learning reveal critical functions of proliferating cells in prognosis and personalized treatment of lung adenocarcinoma.NPJ precision oncology · 2025Article
- Dual phosphorylation of glycogen synthase kinase 3β differentially integrates metabolic programs to determine T cell immunity across vertebrates.Cellular and molecular life sciences : CMLS · 2025Article
- From powerhouse to modulator: regulating immune system responses through intracellular mitochondrial transfer.Cell communication and signaling : CCS · 2025Review
- Chronological Dynamics of Neuroinflammatory Responses in a High-Fat Diet Mouse Model.International journal of molecular sciences · 2024Article
- Lkb1 orchestrates γδ T-cell metabolic and functional fitness to control IL-17-mediated autoimmune hepatitis.Cellular & molecular immunology · 2024Article
- RhoA balances microglial reactivity and survival during neuroinflammation.Cell death & disease · 2023Article
- Obesity Dysregulates the Immune Response to Influenza Infection and Vaccination Through Metabolic and Inflammatory Mechanisms.Annual review of nutrition · 2022Review
- Review
- Immunometabolic Mechanisms of Heart Failure with Preserved Ejection Fraction.Nature cardiovascular research · 2022Article
- Irgm1 regulates metabolism and function in T cell subsets.Scientific reports · 2022Article
- Neuroprotection offered by mesenchymal stem cells in perinatal brain injury: Role of mitochondria, inflammation, and reactive oxygen species.Journal of neurochemistry · 2021Review
- Interactions of a Water-Soluble Glycofullerene with Glucose Transporter 1. Analysis of the Cellular Effects on a Pancreatic Tumor Model.Nanomaterials (Basel, Switzerland) · 2021Article
- Metabolic adaptations of cells at the vascular-immune interface during atherosclerosis.Molecular aspects of medicine · 2021Article
- Systemic Inflammation Associated with Immune Reconstitution Inflammatory Syndrome in Persons Living with HIV.Life (Basel, Switzerland) · 2021Review
- Review
- Updated Understanding of Cancer as a Metabolic and Telomere-Driven Disease, and Proposal for Complex Personalized Treatment, a Hypothesis.International journal of molecular sciences · 2020Review
- Identification of Immune Response to Sacbrood Virus Infection inFrontiers in genetics · 2020Article
- Metabolic Regulation of Glial Phenotypes: Implications in Neuron-Glia Interactions and Neurological Disorders.Frontiers in cellular neuroscience · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
To engage in proliferation, cells need to increase their biomass and replicate their genome. This process presents a substantial bioenergetic challenge: proliferating cells must increase ATP production and acquire or synthesize raw materials, including lipids, proteins and nucleic acids. To do so, proliferating cells actively reprogramme their intracellular metabolism from catabolic mitochondrial oxidative phosphorylation (OXPHOS) to glycolysis and other anabolic pathways. This metabolic reprogramming, which directs nutrient uptake and metabolism during cell activation and proliferation, is under the control of specific signal transduction pathways. The underlying molecular mechanisms of cell metabolism reprogramming and their relevance to physiology and disease are currently under intense study. Several reports have uncovered the mechanisms of metabolic reprogramming that drive high rates of cell proliferation in cancer. Some recent studies have elucidated the physiological role of metabolic reprogramming during T-cell activation, differentiation and trafficking, which are potentially relevant to inflammatory disorders. This review describes the impact of metabolic reprogramming on the pathogenesis of cancer and the physiology of T-cell-mediated immune responses, with an emphasis on the phosphatidyl inositol 3-kinase-serine/threonine kinase-mammalian target of rapamycin pathway and the recently discovered metabolic processes regulated by nuclear factor-κB. These discoveries will hopefully translate into a better understanding of the role of metabolic reprogramming as a key regulator of T-cell-mediated immune responses and offer novel, immune-based therapeutic approaches.
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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.