ReviewRedox biology2017
Redox regulation in metabolic programming and inflammation.
Review in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 2 of them syntheses that pooled it.
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
138 citing papers in PubMed, 2 syntheses or guidelines pooled it, 272 citations in OpenAlex.
- Mitochondrial dysfunction in sepsis: nutritional strategies for restoring bioenergetic homeostasis.Frontiers in cellular and infection microbiology · 2026Pooled it
- The role of CD36 in immune function: bridging innate and adaptive responses.Frontiers in immunology · 2026Pooled it
- Translating Blue Light Stimulation From Batch to Perfusion: Process and Intracellular Metabolic Analysis.Biotechnology and bioengineering · 2026Article
- Thymoquinone as a Multi-Target Modulator of Inflammatory and Immunometabolic Signaling: Mechanisms and Therapeutic Implications.Cell biochemistry and biophysics · 2026Review
- An epigenetic switch in β-cells links mitochondrial stress to inflammatory fate via HMGB1 acetylation.Cell death and differentiation · 2026Article
- Article
- Ultrasmall Prussian blue-integrated cryogel for enhanced ROS scavenging and immunomodulation via cGAS-STING inhibition in wound healing.Materials today. Bio · 2026Article
- Legumain Restrains Granuloma Formation by Inhibiting mTORC1/STAT1-Mediated M1 Macrophage Polarization in Sarcoidosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- pH-Responsive Cinnamaldehyde-Arginine Nanoprodrug for Targeted Rheumatoid Arthritis Therapy via Antioxidant Activity and Macrophage Reprogramming.Antioxidants (Basel, Switzerland) · 2026Article
- Reactive Oxygen and Nitrogen Species on Monocyte and Macrophage Biology.Antioxidants (Basel, Switzerland) · 2026Review
- Xu Chunfu's Modified Xianglian Pill Regulates the NOX2/ROS/Mitochondria/NLRP3 Axis to Treat Ulcerative Colitis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Targeting mitochondrial bioenergetics: the "Achilles' heel" of Leishmania.Parasites & vectors · 2026Article
- Aortic dissection: the role of macrophages in disease pathogenesis and their potential as a treatment target.Journal of cardiothoracic surgery · 2026Review
- Extracellular Redox Balance as a Determinant of Immune Regulation and Tissue Inflammation.Antioxidants (Basel, Switzerland) · 2026Review
- Nrf2 as a redox checkpoint in autoimmune joint inflammation: microenvironmental redox control across the arthritis spectrum.Frontiers in immunology · 2026Review
- Metabolic Reprogramming and Immune Metabolism in Sepsis: Targeting the PPAR Pathway for Personalized Therapeutic Approaches.PPAR research · 2026Review
- Hemocyanin controlsVirulence · 2025Article
- Scutellarin suppresses Mycobacterium tuberculosis-induced pyroptosis in macrophages by inhibiting the HIF-1α-mediated Warburg effect.Redox report : communications in free radical research · 2025Article
- A redox-dependent switch governing sensory axon degeneration and regeneration.Scientific reports · 2025Article
- Vericiguat reduces pyroptosis in rats with coronary microembolization by inhibiting the AMPK/Nrf2/NLRP3 signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
78 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
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Energy metabolism and redox state are intrinsically linked. In order to mount an adequate immune response, cells must have an adequate and rapidly available energy resource to migrate to the inflammatory site, to generate reactive oxygen species using NADPH as a cofactor and to engulf bacteria or damaged tissue. The first responder cells of the innate immune response, neutrophils, are largely dependent on glycolysis. Neutrophils are relatively short-lived, dying via apoptosis in the process of bacterial killing through production of hypochlorous acid and release of extracellular NETs. Later on, the most prevalent recruited innate immune cells are monocytes. Their role is to complete a damage limitation exercise initiated by neutrophils and then, as re-programmed M2 macrophages, to resolve the inflammatory event. Almost twenty five years ago, it was noted that macrophages lose their glycolytic capacity and become anti-inflammatory after treatment with corticosteroids. In support of this we now understand that, in contrast to early responders, M2 macrophages are predominantly dependent on oxidative phosphorylation for energy. During early inflammation, polarisation towards M1 macrophages is dependent on NOX2 activation which, via protein tyrosine phosphatase oxidation and AKT activation, increases trafficking of glucose transporters to the membrane and consequently increases glucose uptake for glycolysis. In parallel, mitochondrial efficiency is likely to be compromised via nitrosylation of the electron transport chain. Resolution of inflammation is triggered by encounter with apoptotic membranes exposing oxidised phosphatidylserine that interact with the scavenger receptor, CD36. Downstream of CD36, activation of AMPK and PPARγ elicits mitochondrial biogenesis, arginase expression and a switch towards oxidative phosphorylation in the M2 macrophage. Proinflammatory cytokine production by M2 cells decreases, but anti-inflammatory and wound healing growth factor production is maintained to support restoration of normal function.
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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.