ReviewCellular & molecular biology letters2025
The crucial role of metabolic reprogramming in driving macrophage conversion in kidney disease.
Review in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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Who cites it
18 citing papers in PubMed.
- Single cell multi-omics guided hydrogel enables closed-loop therapy for renal osteodystrophy.Nature communications · 2026Article
- Acute Kidney Injury-to-Chronic Kidney Disease Transition-Associated Macrophage Subtypes: Biological Functions and Intercellular Crosstalk.International journal of molecular sciences · 2026Review
- Article
- Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).International journal of molecular medicine · 2026Review
- Immunological mechanisms and novel therapeutic strategies for sepsis‑associated acute kidney injury (Review).International journal of molecular medicine · 2026Review
- The SPP1-CD44 Signaling Axis Orchestrates Macrophage Metabolism to Promote Early Inflammation in Acute Kidney Injury.International journal of biological sciences · 2026Article
- Mechanisms of Macrophage Glycolytic Reprogramming and Interventional Effects of Traditional Chinese Medicine on Renal Fibrosis.International journal of general medicine · 2026Review
- Precision immunomodulation of viral myocarditis: a spatiotemporal intervention paradigm based on smart biomaterials.Frontiers in immunology · 2026Review
- CD63Frontiers in cellular and infection microbiology · 2026Article
- Residual HIV activity and host immunometabolic remodeling during antiretroviral therapy: implications for cardiovascular-kidney-metabolic risk.Frontiers in immunology · 2026Review
- VISTA Confers Renal Protection in Murine Hemorrhage/Infection-Induced Acute Kidney Injury: Associations with Altered NGAL and HMGB1 Expression.ImmunoTargets and therapy · 2026Article
- Myeloid HIF1α has only a minor impact on atherosclerosis development.Vascular biology (Bristol, England) · 2026Article
- Role of metabolic reprogramming and lactylation in diabetic nephropathy: molecular mechanisms and therapeutic prospects - a narrative review.Frontiers in endocrinology · 2026Review
- Spatiotemporal Double-Edged Sword of Macrophages: Temporal Regulation of Neuroinflammation and Neurorepair in Ischemic Stroke.Journal of immunology research · 2026Review
- Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney.Life (Basel, Switzerland) · 2025Review
- Article
- Rg1-preconditioned adipose-derived mesenchymal stromal cells alleviate colitis via exosome-mediated Inhibition of macrophage glycolysis through RAS signaling.Stem cell research & therapy · 2025Article
- Salvianolic Acid B Attenuates Liver Fibrosis via Suppression of Glycolysis-Dependent m1 Macrophage Polarization.Current issues in molecular biology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Interstitial fibrosis after acute kidney injury is an ongoing pathological process of chronic inflammatory injury and repair. Macrophages participate in renal inflammation, repair and fibrosis by continuously changing their phenotype and function. The tissue microenvironment of kidney injury induces changes in key metabolic enzymes, pathways and metabolites in macrophages, leading to phenotypic and functional conversions, but the detailed mechanisms are unclear. However, in the early phase of acute kidney injury, macrophages shift to a pro-inflammatory role relying on glycolysis and pentose phosphate pathways. The tissue microenvironment regulates the suppression of glycolysis-related genes and the up-regulation of oxidative phosphorylation and tricarboxylic acid cycle genes in macrophages, resulting in a gradual shift to an anti-inflammatory phenotype, which is involved in tissue repair and remodelling. In the late stage of injury, if macrophages continue to be overactive, they will be involved in renal fibrosis. The concomitant enhancement of nucleotide and amino acid metabolism, especially arginine and glutamine metabolism, is critical for the macrophage function and phenotypic transition during the above injury process. Macrophage metabolic reprogramming therefore provides new therapeutic targets for intervention in inflammatory injury and interstitial fibrosis in kidney disease.
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What Socratic 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 Socratic graph.