ReviewHeliyon2023
M2 macrophage polarization in systemic sclerosis fibrosis: pathogenic mechanisms and therapeutic effects.
Review in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed.
- 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
- Loss of Cathepsin Z enhances pro-inflammatory macrophage responses and promotes tissue regeneration.Disease models & mechanisms · 2026Article
- IgA autoantibodies promote inflammation, Th17 polarization and fibrotic responses in hidradenitis suppurativa.Nature communications · 2026Article
- Macrophages Are Critical Inducers of Bleomycin-Induced Fibrosis in a Systemic Scleroderma Model.The American journal of pathology · 2026Article
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- Rubiadin-1-methyl ether alleviates bleomycin induced pulmonary fibrosis.Scientific reports · 2026Article
- Comprehensive analysis of the TGF-β signaling pathway: molecular mechanisms, disease drivers, and frontiers in clinical translation.Frontiers in immunology · 2026Review
- Antibodies against interleukin-10 receptor reduce IL-6 and TNF-α levels and increase TGF-β levels in patients with severe fever with thrombocytopenia syndrome virus and SARS-CoV-2 infection.Frontiers in immunology · 2026Article
- Cardiac sarcoidosis: from clinical manifestations to heart transplantation.Frontiers in medicine · 2026Review
- The immune landscape of systemic sclerosis: from pathogenic mechanisms to precision therapeutic breakthroughs.Frontiers in immunology · 2026Review
- Interactions between neutrophil extracellular traps and macrophages: the key to inflammatory diseases.Frontiers in immunology · 2026Review
- Immunopathogenic Mechanisms in Connective Tissue Disease-Associated Interstitial Lung Disease: Incessant Loop of Immunity to Fibrosis.International journal of molecular sciences · 2025Review
- Article
- Intracellular Calcium as a Regulator of Polarization and Target Reprogramming of Macrophages.International journal of molecular sciences · 2025Review
- Friend or foe? The role of SIRT6 on macrophage polarized to M2 subtype in acute kidney injury to chronic kidney disease.Renal failure · 2025Review
- Targeting the CD47-TSP1 Axis in Abdominal Aortic Aneurysm: A Novel Immunotherapeutic Approach.International journal of molecular sciences · 2025Review
- Dynamic macrophage phenotypes in autoimmune and inflammatory rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- Inhibition of GDNF-Driven Macrophage-to-Myofibroblast Transition Protects Against Colitis-Associated Intestinal Fibrosis.Inflammation · 2025Article
- [Pathophysiology of fibrosis: inflammatory vs. non-inflammatory].Innere Medizin (Heidelberg, Germany) · 2025Review
- Liver X Receptor-Growth Differentiation Factor 15 Activation Drives Profibrotic Changes in the Aqueous Outflow Tract of Uveitic Glaucoma.The American journal of pathology · 2025Article
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
Systemic sclerosis (SSc, scleroderma), is an autoimmune rheumatic disease characterized by fibrosis of the skin and internal organs, and vasculopathy. Preventing fibrosis by targeting aberrant immune cells that drive extracellular matrix (ECM) over-deposition is a promising therapeutic strategy for SSc. Previous research suggests that M2 macrophages play an essential part in the fibrotic process of SSc. Targeted modulation of molecules that influence M2 macrophage polarization, or M2 macrophages, may hinder the progression of fibrosis. Here, in an effort to offer fresh perspectives on the management of scleroderma and fibrotic diseases, we review the molecular mechanisms underlying the regulation of M2 macrophage polarization in SSc-related organ fibrosis, potential inhibitors targeting M2 macrophages, and the mechanisms by which M2 macrophages participate in fibrosis.
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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.