ReviewInternational journal of general medicine2026
Innovative Insights into Interleukin-Mediated Macrophage Polarization: Metabolic Reprogramming and Inflammatory Pathway Crosstalk in Chronic Kidney Disease and Therapeutic Implications-A Narrative Review.
Review in International journal of general medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Extracellular matrix remodeling and immune reprogramming drive residual tumor progression of liver cancer after incomplete microwave ablation.Molecular oncology · 2026Article
- Single-Cell and Machine Learning Analyses Identify a PFKFB3-Centered Regulatory Network and Potential Salidroside Interaction in Coronary Heart Disease.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: To clarify the molecular mechanisms of interleukin-macrophage polarization axis in reshaping renal inflammatory microenvironment and driving chronic kidney disease (CKD) progression, and explore targeted therapeutic potential. Methods: We systematically searched the PubMed and Embase databases for published studies from January 2015 to March 2026. The search terms used were "chronic kidney disease" or "CKD", "interleukin" or "IL" or "leukocyte protein network", "macrophages" and "inflammation". A total of 186 peer-reviewed studies based on human and animal models were included, with all non-eligible articles excluded in the screening process. Results: Pro-inflammatory interleukins (IL-1β/IL-6/IL-17) orchestrate M1 polarization via multi-pathway crosstalk: IL-1β activates NLRP3 inflammasome to promote IL-18 release, IL-6 binds gp130 to trigger STAT3, and IL-17 activates NF-κB/MAPK, all upregulating glycolytic enzymes (HK2/PFKFB3) and M1 markers (iNOS/CD86). Activated M1 macrophages secrete TNF-α/IL-1β/IL-6, forming an autocrine loop to amplify renal parenchymal injury and monocyte recruitment. Anti-inflammatory interleukins (IL-10/IL-22) induce protective M2 polarization: IL-4 activates STAT6 to upregulate CD206/Arg1, IL-10 inhibits NF-κB, and IL-22 modulates AMPK-mediated mitophagy. However, CKD-induced M2 pathological deviation (elevated TGF-β/CTGF, reduced IL-10) converts reparative functions to profibrotic effects, accelerating glomerulosclerosis. This polarization imbalance forms a vicious cycle with interleukin dysregulation. Targeted interventions show efficacy: tocilizumab (anti-IL-6R) reduces M1 infiltration and urinary albumin; paeoniflorin upregulates IL-10 via KLF4 to induce M2; SGLT2 inhibitors enhance IL-22/AMPK signaling; astragaloside IV promotes IL-4/PPARγ to stabilize M2 polarization, all alleviating inflammation and fibrosis. Conclusion: The interleukin-macrophage polarization axis, regulated by inflammatory pathways and metabolic reprogramming, is a core CKD therapeutic target, supporting multi-target precision interventions.
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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.